Even so, there are many loci (including druggable loci) that alter LDL-C and CAD risk that are expected to have no substantive effect on glycemic status: these include targets of novel therapies that are protein products of PCSK9, APOB and LPA. These findings are reinforced by the persistence of the causal relationship between LDL-C and risk of CAD even after excluding SNPs associated with T2D. The gene discussed is APOB; the disease is type 2 diabetes mellitus.