MiR‐21 was described to ameliorate TGF‐β and hyperglycemia‐induced glomerular injury through repression of pro‐apoptotic signals.34 In contrast to this, murine models of tubule‐interstitial kidney injury demonstrated that miR‐21 contributes to fibrogenesis and epithelial injury.36 In line with these findings, miR‐21 antagonism rescued mesangial expansion, interstitial fibrosis, macrophage infiltration, podocyte loss, albuminuria and fibrotic‐ and inflammatory gene expression in mice with diabetic nephropathy.40 Here, TGFB1 is linked to diabetic kidney disease.