SOAT1 (sterol O-acyltransferase 1) catalyzes the esterification of cholesterol with fatty acids, converting cholesterol into cholesterol esters that are less membrane-soluble, thereby regulating cellular cholesterol homeostasis 1. The enzyme preferentially utilizes oleoyl-CoA as a substrate, showing highest activity toward acyl-CoA with a delta-9 position double bond 2. SOAT1 plays critical roles in multiple disease contexts. In hepatocellular carcinoma (HCC), elevated SOAT1 expression characterizes an aggressive subtype associated with poor prognosis; SOAT1 knockdown suppresses HCC proliferation and migration, and SOAT1 inhibition with avasimibe reduces tumor size in xenograft models 3. SOAT1 promotes HCC development through cholesterol esterification in a P53-deficient context, emerging as both a biomarker and therapeutic target 4. SOAT1 also drives epithelial-mesenchymal transition (EMT) in HCC by disrupting cholesterol metabolism homeostasis, with the natural compound nootkatone showing promise as a SOAT1-targeting inhibitor 5. Beyond HCC, SOAT1 sustains mevalonate pathway dependency in pancreatic cancer by preventing negative feedback from unesterified cholesterol 6. In ferroptosis regulation, SOAT1-mediated cholesterol ester production promotes ferroptotic resistance 7. Additionally, SOAT1 influences macrophage polarization following spinal cord injury; SOAT1 inhibition enhances M2 macrophage polarization and improves functional recovery 8.