This mechanism is anti-atherogenic in normolipidemic individuals, but in cases of hypercholesterolemia and mixed hyperlipidemia, CETP can have a pro-atherogenic role, because of the generation of dense, small and atherogenic LDL [8,9]; elevated levels of apolipoprotein B (ApoB)-containing acceptor particles for CETP lead to enhanced transfer of triglycerides (TG) from very-low-density lipoprotein (VLDL) to HDL, with consequent TG enrichment of HDL and abnormal intravascular metabolism, involving reduction in particle size and decrease of HDL-Cholesterol (-C) and ApoA-I levels [10,11]. Here, CETP is linked to familial hypercholesterolemia.