While LDL-C has been the principal biomarker targeted for lipid-lowering therapy, accumulating data (including Mendelian randomization studies) demonstrate that all Apolipoprotein B-100 (Apo B) containing lipid particles have a significant role in atherogenesis by facilitating the accumulation of lipid-rich particles within the arterial wall leading to inflammation (now understood as a major drivers of atherosclerosis) [12, 13]. This evidence concerns the gene APOB and atherosclerosis.