In diabetic nephropathy, upregulation of Malat1 promotes renal fibrosis by targeting the miRNA-2355-3p, while in an experimental post-infarct myocardium mouse model, Malat1 mediates cardiac fibrosis by regulating TGF‐β1 activity via miRNA-145 [18, 19]. This evidence concerns the gene TGFB1 and renal fibrosis.