{"gene":"FLT3LG","run_date":"2026-06-09T23:54:43","timeline":{"discoveries":[{"year":2021,"finding":"Full-length natural Flt3Lg serves as a functional recognition module for Flt3 receptor on AML cells; Flt3-CAR T cells using Flt3Lg as the extracellular targeting domain specifically killed Flt3-positive THP-1 cells but not Flt3-negative U937 cells, and this killing was competitively inhibited by soluble Flt3-ligand in a dose-dependent manner.","method":"In vitro cytotoxicity assay with CAR T cells, competitive inhibition with soluble Flt3Lg, Flt3-positive vs. Flt3-negative cell line comparison","journal":"Vaccines","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — specific functional assay with orthogonal controls (Flt3-negative cells, competitive inhibition), single lab","pmids":["34835169"],"is_preprint":false},{"year":2023,"finding":"A single L27P point mutation in Flt3Lg reduces its bioactivity (ED50 at least 10-fold higher than wild-type Flt3Lg produced in CHO cells) and reduces Flt3 recycling, while retaining specificity for Flt3 receptor binding when used as the extracellular domain of a CAR construct.","method":"Recombinant protein production in CHO cells, ED50 bioactivity assay, Flt3 recycling assay, CAR T-cell specificity assay","journal":"International journal of molecular sciences","confidence":"Medium","confidence_rationale":"Tier 1–2 / Moderate — in vitro assay with mutagenesis and functional readout, single lab","pmids":["37108788"],"is_preprint":false},{"year":2024,"finding":"FLT3LG can directly act on CD8+ T cells to promote their proliferation and activation; FLT3LG synergizes with T-cell receptor activators to promote activation of tumor-derived T cells in vitro, and FLT3 inhibitors neutralize the antitumor effects of BCG immunotherapy.","method":"In vitro T-cell proliferation and activation assay, FLT3 inhibitor treatment, BCG stimulation model","journal":"Journal of Cancer","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — in vitro functional assay with pharmacological inhibition as orthogonal control, single lab","pmids":["38213738"],"is_preprint":false},{"year":2026,"finding":"NK cell production of FLT3LG is regulated by IL2 and IL15 signaling; specifically, IL2 signaling in NK cells uniquely induces Flt3L expression, and CD11b-CD27+ NK cell subsets are enriched for IL2 family signaling and upregulate Flt3l upon activation. Increased NK cell-derived Flt3L boosts conventional type I dendritic cell (cDC1) abundance in the tumor and improves anti-PD-1 immunotherapy response in melanoma.","method":"Mouse melanoma model, NK cell subset analysis, IL2/IL15 stimulation, cDC1 abundance quantification, anti-PD-1 treatment outcome measurement, correlation with human melanoma datasets","journal":"Cancer immunology research","confidence":"Medium","confidence_rationale":"Tier 2 / Moderate — in vivo mouse model with defined genetic/cytokine perturbation and multiple functional readouts, single lab but supported by human dataset correlation","pmids":["41081432"],"is_preprint":false},{"year":2020,"finding":"FLT3LG binds to FLT3 on dendritic cells to stimulate their differentiation and expansion, facilitating tumor antigen cross-presentation and anticancer immune responses.","method":"Review/commentary citing established mechanism (no new primary experiment described)","journal":"Oncoimmunology","confidence":"Low","confidence_rationale":"Tier 4 / Weak — mechanistic claim stated as established background in a commentary, no primary experimental data presented in this paper","pmids":["32363127"],"is_preprint":false}],"current_model":"FLT3LG is a ligand for the FLT3 receptor tyrosine kinase that binds FLT3 on dendritic cells to stimulate their differentiation and expansion (facilitating antigen cross-presentation), directly activates CD8+ T cells in synergy with TCR signals, and is produced by NK cells under IL2/IL15 signaling to control cDC1 abundance in tumors and enhance anti-PD-1 immunotherapy; a single L27P mutation reduces its bioactivity at least 10-fold while retaining receptor binding specificity."},"narrative":{"mechanistic_narrative":"FLT3LG is the cognate ligand for the FLT3 receptor and functions in dendritic cell biology and antitumor immunity by engaging FLT3 to drive dendritic cell differentiation and expansion [PMID:34835169, PMID:32363127]. Its FLT3-binding module is sufficiently specific that full-length FLT3LG can serve as the extracellular targeting domain of a chimeric antigen receptor, killing FLT3-positive but not FLT3-negative cells in a manner competitively inhibited by soluble ligand [PMID:34835169]. A single L27P substitution reduces bioactivity at least 10-fold and impairs FLT3 receptor recycling while preserving receptor-binding specificity, dissociating the binding and signaling-competent functions of the ligand [PMID:37108788]. Beyond dendritic cells, FLT3LG acts directly on CD8+ T cells to promote proliferation and activation and synergizes with T-cell receptor stimulation, contributing to the antitumor effects of BCG immunotherapy [PMID:38213738]. NK cells are a regulated cellular source of FLT3LG: IL2 signaling uniquely induces its expression, and NK cell-derived FLT3LG increases intratumoral cDC1 abundance and improves anti-PD-1 immunotherapy response [PMID:41081432].","teleology":[{"year":2020,"claim":"Established the core mechanistic role of FLT3LG as the FLT3 ligand driving dendritic cell differentiation/expansion and tumor antigen cross-presentation, framing it as a node in anticancer immunity.","evidence":"Review/commentary citing established receptor-ligand mechanism, no new primary experiment","pmids":["32363127"],"confidence":"Low","gaps":["No new primary experimental data presented in this source","Does not quantify the contribution of FLT3LG to cross-presentation directly","Cell-intrinsic signaling consequences not addressed"]},{"year":2021,"claim":"Demonstrated that the FLT3-binding module of FLT3LG is specific and exploitable, showing full-length FLT3LG can redirect CAR T cells to FLT3-positive targets.","evidence":"In vitro CAR T-cell cytotoxicity assay with FLT3-positive vs FLT3-negative cell lines and competitive inhibition by soluble ligand","pmids":["34835169"],"confidence":"Medium","gaps":["Specificity shown only in cell lines, not in vivo","Does not map the binding interface residues","Single lab"]},{"year":2023,"claim":"Separated FLT3LG receptor binding from downstream bioactivity by showing a single L27P mutation cripples potency and receptor recycling while preserving binding specificity.","evidence":"Recombinant CHO-produced protein, ED50 bioactivity assay, FLT3 recycling assay, CAR specificity assay","pmids":["37108788"],"confidence":"Medium","gaps":["Structural basis of the recycling defect not resolved","Effect on natural dendritic cell expansion not tested","Single lab"]},{"year":2024,"claim":"Extended FLT3LG function beyond dendritic cells by showing it acts directly on CD8+ T cells and synergizes with TCR signals, linking it to BCG immunotherapy efficacy.","evidence":"In vitro T-cell proliferation/activation assays, FLT3 inhibitor neutralization, BCG stimulation model","pmids":["38213738"],"confidence":"Medium","gaps":["Whether FLT3 is expressed and signals directly on these T cells not fully resolved","In vivo contribution distinct from dendritic cell effects unclear","Single lab"]},{"year":2026,"claim":"Identified NK cells as a cytokine-regulated source of FLT3LG, connecting IL2 signaling to intratumoral cDC1 abundance and anti-PD-1 response.","evidence":"Mouse melanoma model with NK subset analysis, IL2/IL15 stimulation, cDC1 quantification, anti-PD-1 outcomes, human dataset correlation","pmids":["41081432"],"confidence":"Medium","gaps":["Mechanism of IL2-driven Flt3l transcriptional induction not defined","Relative contribution of NK-derived vs other-source FLT3LG not quantified","Single lab"]},{"year":null,"claim":"The structural determinants of FLT3LG-FLT3 engagement and the signaling pathways activated downstream in dendritic cells versus CD8+ T cells remain undefined in the available corpus.","evidence":"","pmids":[],"confidence":"Medium","gaps":["No structural model of the FLT3LG-FLT3 complex in the timeline","Downstream signaling cascade not characterized","Transcriptional regulation of FLT3LG expression beyond IL2 not mapped"]}],"mechanism_profile":{"molecular_activity":[{"term_id":"GO:0048018","term_label":"receptor ligand activity","supporting_discovery_ids":[0,1,4]}],"localization":[],"pathway":[{"term_id":"R-HSA-168256","term_label":"Immune System","supporting_discovery_ids":[2,3,4]}],"complexes":[],"partners":["FLT3"],"other_free_text":[]}},"prefetch_data":{"uniprot":{"accession":"P49771","full_name":"Fms-related tyrosine kinase 3 ligand","aliases":["SL cytokine"],"length_aa":235,"mass_kda":26.4,"function":"Stimulates the proliferation of early hematopoietic cells by activating FLT3. Synergizes well with a number of other colony stimulating factors and interleukins. Required for the development of B cells, and dendritic cells (DCs)","subcellular_location":"Secreted","url":"https://www.uniprot.org/uniprotkb/P49771/entry"},"depmap":{"release":"DepMap","has_data":true,"is_common_essential":false,"resolved_as":"","url":"https://depmap.org/portal/gene/FLT3LG","classification":"Not Classified","n_dependent_lines":23,"n_total_lines":1208,"dependency_fraction":0.01903973509933775},"opencell":{"profiled":false,"resolved_as":"","ensg_id":"","cell_line_id":"","localizations":[],"interactors":[],"url":"https://opencell.sf.czbiohub.org/search/FLT3LG","total_profiled":1310},"omim":[{"mim_id":"620926","title":"IMMUNODEFICIENCY 125; IMD125","url":"https://www.omim.org/entry/620926"},{"mim_id":"614172","title":"IMMUNODEFICIENCY 21; IMD21","url":"https://www.omim.org/entry/614172"},{"mim_id":"610049","title":"SAP DOMAIN-CONTAINING RIBONUCLEOPROTEIN; SARNP","url":"https://www.omim.org/entry/610049"},{"mim_id":"605384","title":"INTERLEUKIN 21; IL21","url":"https://www.omim.org/entry/605384"},{"mim_id":"601728","title":"PHOSPHATASE AND TENSIN HOMOLOG; PTEN","url":"https://www.omim.org/entry/601728"}],"hpa":{"profiled":true,"resolved_as":"","reliability":"","locations":[],"tissue_specificity":"Low tissue specificity","tissue_distribution":"Detected in all","driving_tissues":[],"url":"https://www.proteinatlas.org/search/FLT3LG"},"hgnc":{"alias_symbol":[],"prev_symbol":[]},"alphafold":{"accession":"P49771","domains":[{"cath_id":"1.20.1250.10","chopping":"39-154","consensus_level":"high","plddt":97.4127,"start":39,"end":154}],"viewer_url":"https://alphafold.ebi.ac.uk/entry/P49771","model_url":"https://alphafold.ebi.ac.uk/files/AF-P49771-F1-model_v6.cif","pae_url":"https://alphafold.ebi.ac.uk/files/AF-P49771-F1-predicted_aligned_error_v6.png","plddt_mean":81.31},"mouse_models":{"mgi_url":"https://www.informatics.jax.org/marker/summary?nomen=FLT3LG","jax_strain_url":"https://www.jax.org/strain/search?query=FLT3LG"},"sequence":{"accession":"P49771","fasta_url":"https://rest.uniprot.org/uniprotkb/P49771.fasta","uniprot_url":"https://www.uniprot.org/uniprotkb/P49771/entry","alphafold_viewer_url":"https://alphafold.ebi.ac.uk/entry/P49771"}},"corpus_meta":[{"pmid":"32363127","id":"PMC_32363127","title":"FLT3LG - a biomarker reflecting clinical responses to the immunogenic cell death inducer oxaliplatin.","date":"2020","source":"Oncoimmunology","url":"https://pubmed.ncbi.nlm.nih.gov/32363127","citation_count":24,"is_preprint":false},{"pmid":"34835169","id":"PMC_34835169","title":"Natural Flt3Lg-Based Chimeric Antigen Receptor (Flt3-CAR) T Cells Successfully Target Flt3 on AML Cell Lines.","date":"2021","source":"Vaccines","url":"https://pubmed.ncbi.nlm.nih.gov/34835169","citation_count":19,"is_preprint":false},{"pmid":"40329265","id":"PMC_40329265","title":"FLT3LG modulates the infiltration of immune cells and enhances the efficacy of anti-PD-1 therapy in lung adenocarcinoma.","date":"2025","source":"BMC cancer","url":"https://pubmed.ncbi.nlm.nih.gov/40329265","citation_count":6,"is_preprint":false},{"pmid":"38213738","id":"PMC_38213738","title":"BCG immunotherapy promotes tumor-derived T-cell activation through the FLT3/FLT3LG pathway in bladder cancer.","date":"2024","source":"Journal of Cancer","url":"https://pubmed.ncbi.nlm.nih.gov/38213738","citation_count":5,"is_preprint":false},{"pmid":"37108788","id":"PMC_37108788","title":"Mutated Flt3Lg Provides Reduced Flt3 Recycling Compared to Wild-Type Flt3Lg and Retains the Specificity of Flt3Lg-Based CAR T-Cell Targeting in AML Models.","date":"2023","source":"International journal of molecular sciences","url":"https://pubmed.ncbi.nlm.nih.gov/37108788","citation_count":4,"is_preprint":false},{"pmid":"41081432","id":"PMC_41081432","title":"IL2/IL15 Signaling Induces NK Cell Production of FLT3LG, Augmenting Anti-PD-1 Immunotherapy.","date":"2026","source":"Cancer immunology research","url":"https://pubmed.ncbi.nlm.nih.gov/41081432","citation_count":1,"is_preprint":false},{"pmid":"41152656","id":"PMC_41152656","title":"FLT3LG as an inflammatory hub bridging tumor immune surveillance to therapy response in breast cancer.","date":"2025","source":"Clinical and experimental medicine","url":"https://pubmed.ncbi.nlm.nih.gov/41152656","citation_count":0,"is_preprint":false},{"pmid":"42208361","id":"PMC_42208361","title":"Highlighting the changes of the Lymphocyte-to-Monocyte ratio in B-cell non-Hodgkin Lymphoma with the treatment and its association with the FLT3/FLT3LG system.","date":"2026","source":"Immunobiology","url":"https://pubmed.ncbi.nlm.nih.gov/42208361","citation_count":0,"is_preprint":false},{"pmid":null,"id":"bio_10.1101_2024.10.25.620123","title":"Analysis of the progression of cervical cancer in Guatemala- from pre-malignancy to invasive disease","date":"2024-10-29","source":"bioRxiv","url":"https://doi.org/10.1101/2024.10.25.620123","citation_count":0,"is_preprint":true}],"cost":{"stage1":{"model":"claude-sonnet-4-6","input_tokens":6680,"output_tokens":1299,"usd":0.019762,"stage1_stop_reason":"end_turn"},"stage2":{"model":"claude-opus-4-8","input_tokens":7936,"output_tokens":1972,"usd":0.04449,"stage2_stop_reason":"end_turn"},"total_usd":0.064252,"stage1_batch_id":"msgbatch_01AsR7g8dGTEiEw9U83bJeWn","stage2_batch_id":"msgbatch_01YV5ZyxtFNUZEjxRcpd9jzb","note":"batch pricing = 50% of standard"},"stage1_raw":"```json\n{\n  \"discoveries\": [\n    {\n      \"year\": 2021,\n      \"finding\": \"Full-length natural Flt3Lg serves as a functional recognition module for Flt3 receptor on AML cells; Flt3-CAR T cells using Flt3Lg as the extracellular targeting domain specifically killed Flt3-positive THP-1 cells but not Flt3-negative U937 cells, and this killing was competitively inhibited by soluble Flt3-ligand in a dose-dependent manner.\",\n      \"method\": \"In vitro cytotoxicity assay with CAR T cells, competitive inhibition with soluble Flt3Lg, Flt3-positive vs. Flt3-negative cell line comparison\",\n      \"journal\": \"Vaccines\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — specific functional assay with orthogonal controls (Flt3-negative cells, competitive inhibition), single lab\",\n      \"pmids\": [\"34835169\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2023,\n      \"finding\": \"A single L27P point mutation in Flt3Lg reduces its bioactivity (ED50 at least 10-fold higher than wild-type Flt3Lg produced in CHO cells) and reduces Flt3 recycling, while retaining specificity for Flt3 receptor binding when used as the extracellular domain of a CAR construct.\",\n      \"method\": \"Recombinant protein production in CHO cells, ED50 bioactivity assay, Flt3 recycling assay, CAR T-cell specificity assay\",\n      \"journal\": \"International journal of molecular sciences\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 1–2 / Moderate — in vitro assay with mutagenesis and functional readout, single lab\",\n      \"pmids\": [\"37108788\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2024,\n      \"finding\": \"FLT3LG can directly act on CD8+ T cells to promote their proliferation and activation; FLT3LG synergizes with T-cell receptor activators to promote activation of tumor-derived T cells in vitro, and FLT3 inhibitors neutralize the antitumor effects of BCG immunotherapy.\",\n      \"method\": \"In vitro T-cell proliferation and activation assay, FLT3 inhibitor treatment, BCG stimulation model\",\n      \"journal\": \"Journal of Cancer\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — in vitro functional assay with pharmacological inhibition as orthogonal control, single lab\",\n      \"pmids\": [\"38213738\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2026,\n      \"finding\": \"NK cell production of FLT3LG is regulated by IL2 and IL15 signaling; specifically, IL2 signaling in NK cells uniquely induces Flt3L expression, and CD11b-CD27+ NK cell subsets are enriched for IL2 family signaling and upregulate Flt3l upon activation. Increased NK cell-derived Flt3L boosts conventional type I dendritic cell (cDC1) abundance in the tumor and improves anti-PD-1 immunotherapy response in melanoma.\",\n      \"method\": \"Mouse melanoma model, NK cell subset analysis, IL2/IL15 stimulation, cDC1 abundance quantification, anti-PD-1 treatment outcome measurement, correlation with human melanoma datasets\",\n      \"journal\": \"Cancer immunology research\",\n      \"confidence\": \"Medium\",\n      \"confidence_rationale\": \"Tier 2 / Moderate — in vivo mouse model with defined genetic/cytokine perturbation and multiple functional readouts, single lab but supported by human dataset correlation\",\n      \"pmids\": [\"41081432\"],\n      \"is_preprint\": false\n    },\n    {\n      \"year\": 2020,\n      \"finding\": \"FLT3LG binds to FLT3 on dendritic cells to stimulate their differentiation and expansion, facilitating tumor antigen cross-presentation and anticancer immune responses.\",\n      \"method\": \"Review/commentary citing established mechanism (no new primary experiment described)\",\n      \"journal\": \"Oncoimmunology\",\n      \"confidence\": \"Low\",\n      \"confidence_rationale\": \"Tier 4 / Weak — mechanistic claim stated as established background in a commentary, no primary experimental data presented in this paper\",\n      \"pmids\": [\"32363127\"],\n      \"is_preprint\": false\n    }\n  ],\n  \"current_model\": \"FLT3LG is a ligand for the FLT3 receptor tyrosine kinase that binds FLT3 on dendritic cells to stimulate their differentiation and expansion (facilitating antigen cross-presentation), directly activates CD8+ T cells in synergy with TCR signals, and is produced by NK cells under IL2/IL15 signaling to control cDC1 abundance in tumors and enhance anti-PD-1 immunotherapy; a single L27P mutation reduces its bioactivity at least 10-fold while retaining receptor binding specificity.\"\n}\n```","stage2_raw":"{\n  \"mechanistic_narrative\": \"FLT3LG is the cognate ligand for the FLT3 receptor and functions in dendritic cell biology and antitumor immunity by engaging FLT3 to drive dendritic cell differentiation and expansion [#0, #4]. Its FLT3-binding module is sufficiently specific that full-length FLT3LG can serve as the extracellular targeting domain of a chimeric antigen receptor, killing FLT3-positive but not FLT3-negative cells in a manner competitively inhibited by soluble ligand [#0]. A single L27P substitution reduces bioactivity at least 10-fold and impairs FLT3 receptor recycling while preserving receptor-binding specificity, dissociating the binding and signaling-competent functions of the ligand [#1]. Beyond dendritic cells, FLT3LG acts directly on CD8+ T cells to promote proliferation and activation and synergizes with T-cell receptor stimulation, contributing to the antitumor effects of BCG immunotherapy [#2]. NK cells are a regulated cellular source of FLT3LG: IL2 signaling uniquely induces its expression, and NK cell-derived FLT3LG increases intratumoral cDC1 abundance and improves anti-PD-1 immunotherapy response [#3].\",\n  \"teleology\": [\n    {\n      \"year\": 2020,\n      \"claim\": \"Established the core mechanistic role of FLT3LG as the FLT3 ligand driving dendritic cell differentiation/expansion and tumor antigen cross-presentation, framing it as a node in anticancer immunity.\",\n      \"evidence\": \"Review/commentary citing established receptor-ligand mechanism, no new primary experiment\",\n      \"pmids\": [\"32363127\"],\n      \"confidence\": \"Low\",\n      \"gaps\": [\"No new primary experimental data presented in this source\", \"Does not quantify the contribution of FLT3LG to cross-presentation directly\", \"Cell-intrinsic signaling consequences not addressed\"]\n    },\n    {\n      \"year\": 2021,\n      \"claim\": \"Demonstrated that the FLT3-binding module of FLT3LG is specific and exploitable, showing full-length FLT3LG can redirect CAR T cells to FLT3-positive targets.\",\n      \"evidence\": \"In vitro CAR T-cell cytotoxicity assay with FLT3-positive vs FLT3-negative cell lines and competitive inhibition by soluble ligand\",\n      \"pmids\": [\"34835169\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Specificity shown only in cell lines, not in vivo\", \"Does not map the binding interface residues\", \"Single lab\"]\n    },\n    {\n      \"year\": 2023,\n      \"claim\": \"Separated FLT3LG receptor binding from downstream bioactivity by showing a single L27P mutation cripples potency and receptor recycling while preserving binding specificity.\",\n      \"evidence\": \"Recombinant CHO-produced protein, ED50 bioactivity assay, FLT3 recycling assay, CAR specificity assay\",\n      \"pmids\": [\"37108788\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Structural basis of the recycling defect not resolved\", \"Effect on natural dendritic cell expansion not tested\", \"Single lab\"]\n    },\n    {\n      \"year\": 2024,\n      \"claim\": \"Extended FLT3LG function beyond dendritic cells by showing it acts directly on CD8+ T cells and synergizes with TCR signals, linking it to BCG immunotherapy efficacy.\",\n      \"evidence\": \"In vitro T-cell proliferation/activation assays, FLT3 inhibitor neutralization, BCG stimulation model\",\n      \"pmids\": [\"38213738\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Whether FLT3 is expressed and signals directly on these T cells not fully resolved\", \"In vivo contribution distinct from dendritic cell effects unclear\", \"Single lab\"]\n    },\n    {\n      \"year\": 2026,\n      \"claim\": \"Identified NK cells as a cytokine-regulated source of FLT3LG, connecting IL2 signaling to intratumoral cDC1 abundance and anti-PD-1 response.\",\n      \"evidence\": \"Mouse melanoma model with NK subset analysis, IL2/IL15 stimulation, cDC1 quantification, anti-PD-1 outcomes, human dataset correlation\",\n      \"pmids\": [\"41081432\"],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"Mechanism of IL2-driven Flt3l transcriptional induction not defined\", \"Relative contribution of NK-derived vs other-source FLT3LG not quantified\", \"Single lab\"]\n    },\n    {\n      \"year\": null,\n      \"claim\": \"The structural determinants of FLT3LG-FLT3 engagement and the signaling pathways activated downstream in dendritic cells versus CD8+ T cells remain undefined in the available corpus.\",\n      \"evidence\": \"\",\n      \"pmids\": [],\n      \"confidence\": \"Medium\",\n      \"gaps\": [\"No structural model of the FLT3LG-FLT3 complex in the timeline\", \"Downstream signaling cascade not characterized\", \"Transcriptional regulation of FLT3LG expression beyond IL2 not mapped\"]\n    }\n  ],\n  \"mechanism_profile\": {\n    \"molecular_activity\": [\n      {\"term_id\": \"GO:0048018\", \"supporting_discovery_ids\": [0, 1, 4]}\n    ],\n    \"localization\": [],\n    \"pathway\": [\n      {\"term_id\": \"R-HSA-168256\", \"supporting_discovery_ids\": [2, 3, 4]}\n    ],\n    \"complexes\": [],\n    \"partners\": [\"FLT3\"],\n    \"other_free_text\": []\n  }\n}","audit_flag":null,"evaluation":{"pairwise":"win","faith_supported":5,"faith_total":5,"faith_pct":100.0}}