MERTK is a receptor tyrosine kinase that functions as a master regulator of efferocytosis and immune homeostasis. Upon ligand binding (including GAS6, LGALS3, TUB, or TULP1), MERTK undergoes autophosphorylation and recruits downstream signaling molecules like GRB2 and PLCG2, activating MAPK and FAK/PTK2 pathways 1. In the retina, MERTK mediates rod outer segment phagocytosis by retinal pigment epithelium cells, and mutations cause retinitis pigmentosa 38. Beyond ocular function, MERTK plays critical roles in multiple disease contexts: MERTK-expressing macrophages promote lung fibrosis in idiopathic pulmonary fibrosis 2, and macrophage MERTK drives hepatic stellate cell activation and liver fibrosis in nonalcoholic steatohepatitis via ERK-TGFβ1 signaling 3. MERTK also regulates stroke outcome by mediating synapse engulfment during reactive gliosis, with MERTK inhibition improving neurobehavioral outcomes 4. Pharmacological MERTK inhibition reduces organ fibrosis across liver, kidney, and lung models by disrupting TGFβ positive feedback loops 5. Additionally, MERTK-mediated efferocytosis in macrophages constrains liver regeneration through NLRP3 inflammasome activation 6, and MERTK functions in glucose homeostasis as the receptor for the myokine feimin, with genetic variants impairing glucose control 7. These findings establish MERTK as a multifunctional therapeutic target across fibrotic, neurological, metabolic, and regenerative diseases.