Atherosclerosis, the pathological foundation of CCVD, is characterized by lipid buildup, fibrosis, and calcification of the arterial wall, resulting in hemodynamic alterations and vessel lumen narrowing.[17] LDL-C is thought to be the most significant lipid marker for the risk of CCVD in this process.[18,19] However, in recent years, it has been discovered that leftover cholesterol might enter the artery wall, harm the intima, and cause atherosclerosis, which in turn can lead to CCVD.[20] Furthermore, RCS and inflammation can interact. The gene discussed is COG2; the disease is atherosclerosis.