The observation that in these mice the suppression of sirtuin-3 was associated with the induction of abnormal glycolysis, and that treatment with glycolysis inhibitors ameliorated renal fibrosis and restored sirtuin-3 levels as well, was taken to suggest that the restoration of sirtuin-3 could be a strategy for combating diabetes-associated kidney fibrosis through the inhibition of aberrant glycolysis (Srivastava et al., 2018) (Figure 2). This evidence concerns the gene SIRT3 and diabetes mellitus.