MST1R is a receptor tyrosine kinase located on chromosome 3 that transduces signals from extracellular ligands, primarily MST1, into cellular responses governing survival, migration, and differentiation. Upon ligand binding, MST1R undergoes autophosphorylation and recruits downstream effectors including PIK3R1, PLCG1, and GAB1, activating signaling cascades including RAS-ERK, PI3K-AKT, and PLCγ-PKC pathways 1. The receptor plays critical roles in wound healing through epithelial cell migration and proliferation, and in innate immunity by regulating macrophage migration and phagocytosis. MST1R dysfunction is implicated in multiple diseases. In cancer, MST1R is overexpressed in >80% of pancreatic cancers 2, where it accelerates progression through effects on both epithelial cells and tumor-associated macrophages. Similar roles exist in breast cancer, where RON/HGFL co-overexpression promotes tumorigenesis via autocrine and paracrine mechanisms 1. A FAK/c-MET/MST1R protein panel risk-stratifies colorectal cancer patients 3. MST1R also associates with nasopharyngeal carcinoma and melanoma progression 4. Beyond malignancy, MST1R variants contribute to premature ovarian insufficiency 5 and tetralogy of Fallot, where MST1R-deficient induced pluripotent stem cells differentiate into non-functional cardiomyocytes 6. Recent evidence identifies MST1R as a druggable target for osteoarthritis 7.