We aimed to characterize in greater detail the impact of variation at this locus and its role in triglyceride metabolism as seen from an epidemiological perspective, including elucidating APOC3’s LPL-dependent and LPL-independent actions on the levels and composition of specific lipoprotein particles, as well as the mechanism of action of a recently proposed APOC3 inhibitor for the treatment of hypertriglyceridemia. This evidence concerns the gene LPL and hypertriglyceridemia.