Besseling et al. included HeFH only with a confirmed pathogenic mutation, and found a dose-dependent association in HeFH subjects with LDLR negative mutations who had a lower T2DM prevalence than HeFH carriers of defective LDLR or APOB mutations, suggesting that the severity of the genetic defect plays a role in T2DM protection4. This evidence concerns the gene LDLR and type 2 diabetes mellitus.