Studies on Apoe −/− mice underscore the deleterious effects of macrophage-specific PLAU overexpression, leading to accelerated atherosclerosis, coronary artery occlusion, and premature demise.[42] Notably, a strong association between PLAU and acute myocardial infarction has been elucidated, particularly evidenced by the SNP rs4065 in the Chinese Han population.[43] CLEC2B, belonging to the C-type lectin domain family 2, encodes members of the C-type lectin/C-type lectin-like domain (CTL/CTLD) superfamily. Here, APOE is linked to arterial occlusion.