Five years ago, the R3i identified atherogenic dyslipidaemia, defined as the imbalance between proatherogenic apoB-containing lipoproteins (contained in triglyceride-rich lipoproteins, TRLs) and antiatherogenic apo A-I-lipoproteins (contained in HDL), as a key contributor to residual CV risk [7]. This evidence concerns the gene APOB and inherited lipid metabolism disorder.