Firstly, some genetic disorders raise HDL cholesterol, such as primary familial or secondary hyperalphalipoproteinemia, mainly resulting in the overproduction or variants of apolipoprotein C-III (Apo-C III) due to a mutation in Apo-A I. These complications promote HDL cholesterol dysfunction, stimulate smooth muscle cell proliferation, facilitate the interaction between monocytes and endothelial cells, and alter platelet activity, all triggering atherosclerosis [298,299,301]. Here, APOC3 is linked to atherosclerosis.