Genetic predisposition plays an important role, as evidenced by genome-wide association studies (GWAS) identifying over 150 loci linked to ASCVD, including mutations in LDL receptor (LDLR), apolipoprotein B-100 (ApoB), and proprotein convertase subtilisin/kexin type-9 (PCSK9) that influence lipid metabolism [10,11]. Here, APOB is linked to atherosclerosis.