This has been demonstrated by Ference et al., who found that for three mechanisms–HMGCR, proprotein convertase subtilisin/kexin type 9 (PCSK9) and low-density lipoprotein receptor (LDLR)–‘each set of gene-specific variants ... had a very similar effect as the other sets on the risk of diabetes per unit decrease in the LDL cholesterol level’.27 This evidence concerns the gene LDLR and diabetes mellitus.