APOF (apolipoprotein F) is a minor apolipoprotein primarily synthesized in the liver 1 that plays a multifaceted role in lipoprotein metabolism and disease pathogenesis. Its primary function involves inhibiting cholesteryl ester transfer protein (CETP) activity and regulating plasma triglyceride-rich lipoprotein metabolism 2. APOF binds preferentially to LDL particles, with binding capacity determined by LDL particle size 3. Mechanistically, APOF promotes hepatic VLDL-TG secretion while simultaneously enhancing hepatic lipoprotein remnant clearance through increased expression of receptors like LDLR and LRP1 2. Transcriptionally, APOF expression is regulated by ETS-1/ETS-2 and C/EBPα transcription factors acting synergistically 1. Disease relevance is substantial: elevated plasma APOF levels associate with increased psoriasis risk 45, and APOF appears to contribute to metabolic-associated steatohepatitis (MASH) progression, serving as a component of the APASHA predictive model for MASH stratification 6. Pan-cancer analysis revealed APOF's differential expression in multiple cancer types with prognostic implications 7. In hyperlipidemic states, APOF levels and binding capacity are differentially altered, with hypertriglyceridemia reducing LDL-bound APOF by >80% 3. These findings establish APOF as a key regulator of lipid homeostasis with emerging importance in metabolic and inflammatory disease pathogenesis.