In the last decade, several HDL‐C candidate genes have been identified via association studies and one of the candidate genes found to be associated in GWAS is LIPG. Studies using genetically modified mice have suggested that LIPG activity negatively influences plasma HDL‐C levels.16, 17 The high‐level overexpression of LIPG in the liver significantly decreased the levels of serum HDL‐C and ApoA1.17 A relevant study showed that the LIPG mutations are involved in increased monocyte adhesion and uptake in the vessel wall, which is used to indicate the early inflammation step of atherosclerosis. Here, APOA1 is linked to atherosclerosis.