Additionally, according to Li et al., melatonin was used to ameliorate TGF-β1-induced renal fibroblast to myofibroblast transdifferentiation (FMT) and UUO-induced renal fibrosis by decreasing the levels of α-SMA, collagen-I, fibronectin, and miR-21-5p and the phosphorylation of STAT3 and by increasing the expressions of Spry1 and PTEN (Li et al., 2020a). The gene discussed is STAT3; the disease is renal fibrosis.