Different studies have reported differentially modulated ApoC‐III proteoforms in isolated lipoproteins as result of metabolic disease (MetS and T2DM) but with contrasting results (showing higher, lower and not significantly different levels of these proteins [52, 53, 54]) probably due to different strategies for normalisation (expressed as percentage to total ApoC‐III, or normalised against the lead apolipoprotein of a specific lipoprotein fraction i.e. ApoB or ApoA‐I). The gene discussed is APOB; the disease is metabolic syndrome.