The TGF‐β/Smad3 signaling pathway is the primary regulator of MMT during kidney fibrosis.[26] Smad3 is not only a central mediator of TGF‐β signaling in fibrotic diseases, but its deficiency also significantly inhibits the transition of tumor‐associated macrophages into tumor‐associated fibroblasts.[27] Targeting Smad3 activity is thus considered a potential antifibrotic therapeutic strategy.[28, 29] To investigate the regulatory role of Smad3 in the UCP2‐mediated MMT process during CP, we induced the MMT phenotype in BMDMs and assessed Smad3 expression levels. The gene discussed is UCP2; the disease is neoplasm.