Given the multifactorial nature of FCH, with other genetic or environmental factors (e.g., obesity) causing an increase in the hepatic production of lipoproteins, the catabolic capacity of LPL in individuals who are genetically predisposed to a low basal level of LPL activity may be overwhelmed, exacerbating the primary dyslipidemia and thus accelerating atherosclerosis [23]. This evidence concerns the gene LPL and atherosclerosis.