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. Here, TGFB1 is linked to neoplasm.