The increased activity of LPL provides a phospholipid source for HDL particles, while PPARα also increases the expression of ABCA1, ABCG1, and type I Class B scavenger receptor (SR-BI), promotes cholesterol effluents from macrophages and selective uptake of cholesterol ester by the liver, accelerates the reverse cholesterol transport, and reduces the accumulation of cholesterol in the body and the risk of cardiovascular diseases [34]. The gene discussed is PPARA; the disease is cardiovascular disorder.