Although the design of our study cannot address the mechanism by which antiretroviral treatment and HIV-infection interact with the polymorphism, it could be argued that antiretroviral treatment may interfere in the functioning of lipolytic enzymes, [29,30] which are regulated by serum apo C-III concentrations, decreasing the catabolism of triglyceride-rich proteins in carriers of the rs10892151 A allele. Here, APOC3 is linked to HIV infectious disease.