DNA methylation could be inherited by progeny, which could explain the perpetuation of myofibroblast activation.177 Moreover, hypermethylation of antifibrotic genes like secreted frizzled-related proteins 5 (sFRP5),178 KLOTHO,179,180 and Krüppel-like factor 4 (KLF4) also contribute to renal fibrosis.181 Collectively, targeting DNA methylation might be a therapeutic strategy, as RASAL1 hypermethylation could be revoked by bone morphogenic protein 7 (BMP-7), which is a well-known endogenous antagonist of TGF-β.182. This evidence concerns the gene SFRP5 and renal fibrosis.