The pathophysiological significance of BM accumulation in T2DM is not clear, however a robust indication of a causal link between the level of artery BM and cardiovascular disease comes from the highly replicated GWAS-observation of associations between non-coding COL4A1/A2 variants and coronary- and peripheral artery disease [16–18]. This evidence concerns the gene COL4A1 and type 2 diabetes mellitus.