Various mechanisms including fibroblast proliferation, neurohumoral activation, pro-inflammatory cytokine production, oxidative stress, increased myocardial transforming growth factor beta expression, and activation of the advanced glycation end products (AGE)/receptor for AGE (RAGE) axis may contribute to fibrosis in DM, as reviewed in detail elsewhere.91 Cardiac remodelling is often observed in people with DM92,93 and is most likely under-detected because only a few patients with DM undergo CMR imaging. This evidence concerns the gene AGER and diabetes mellitus.