The primary role of LDL-C in disease initiation and progression was supported by data from patients with familial hypercholesterolaemia, who developed atherosclerosis prematurely, and from individuals with variations in PCSK9 (Proprotein Convertase Subtilisin/Kexin Type 9) gene, which is a crucial regulator of plasma cholesterol homeostasis, associated with lifelong low LDL-C levels [5,6]. This evidence concerns the gene PCSK9 and atherosclerosis.