{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMEIS1 is a conserved homeobox transcription factor that plays a pivotal role in developmental processes. Genome‐wide association studies have identified intronic variants in MEIS1 that decrease its expression and are robustly linked to restless legs syndrome (RLS), possibly by perturbing limb development, ferritin/dMT1‐mediated iron metabolism, and neural circuitry. In addition, MEIS1 has been implicated in cardiac conduction, where its association with developmental genes modulates atrial and atrioventricular nodal signaling, and it is increasingly recognized for its contributions to neurodevelopmental conditions such as adolescent idiopathic scoliosis and Tourette syndrome."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the hematopoietic system, MEIS1 functions as a key cofactor with HOX and PBX proteins to govern stem cell renewal, lineage specification, and leukemic transformation. Aberrant overexpression of MEIS1, frequently observed in MLL‐rearranged leukemias, sustains a transcriptional program that fuels cell cycle entry, blocks differentiation, and promotes leukemic cell survival and engraftment. Notably, cooperative interactions between MEIS1 and partners such as HOXA9 or PBX3 are sufficient to transform hematopoietic progenitors, underscoring its central role in initiating and maintaining acute leukemias."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond the hematopoietic compartment, MEIS1 exhibits context‐dependent functions in solid tumors and other tissues. In colorectal and prostate cancers, reduced MEIS1 expression is associated with enhanced tumor growth, chemoresistance, and metastatic behavior, suggesting a tumor‐suppressive role. By contrast, in malignancies such as Ewing sarcoma, super‐enhancer–driven MEIS1 expression collaborates with oncogenic fusion proteins to sustain tumor cell survival. Moreover, mechanistic studies have revealed that MEIS1 integrates extracellular signals through its transcriptional regulatory domains, interacts with cofactors including AP‐2α and RNF20, and is subject to epigenetic regulation—mechanisms that collectively underscore its multifaceted contributions to oncogenesis and highlight its potential as a therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "27", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Juliane Winkelmann, Barbara Schormair, Peter Lichtner, et al. 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