This concords with the pathogenesis of dyslipidemia of which researchers, as stated by Brunzell and Hokanson, hypothesized that “central obesity causes insulin resistance and elevated free fatty acid levels, with the resultant increase in hepatic apoB secretion and increased hepatic lipase activity leading to hypertriglyceridemia, small dense LDL, and decreased HDL” [19]. The gene discussed is APOB; the disease is hypertriglyceridemia.