Renin is known to play a role in myocardial stiffness and contributes to cardiac fibrosis via the renin–angiotensin–aldosterone system.16 The lack of significant differences in other markers is surprising given the plethora of evidence suggesting increased fibroinflammatory markers in diabetes.4 The absence of a more adverse fibroinflammatory profile in this cohort may explain why a similar proportion of our diabetes group had LGE compared with the non-diabetes group even though diabetes is associated with focal cardiac fibrosis as detected by LGE.17 This evidence concerns the gene REN and diabetes mellitus.