Recent studies reported that formononetin attenuates diabetic renal fibrosis by activating the Nrf2/ARE pathway and inactivating the Smad3 pathway, respectively.[25, 26] In our study, we for the first time demonstrated that formononetin could directly bind to PRDM16 and upregulate PRDM16 to promote the expression of TRPA1 to suppress the MAPK/TGF‐β1 axes of renal fibrosis in db/db diabetic mice (Figure 8; Figure S11, Supporting Information). Here, SMAD3 is linked to renal fibrosis.