However, dysregulated repair promotes profibrotic M2a macrophages, which significantly contribute to kidney fibrosis.[10, 11] Recent research has highlighted several significant pathways in renal fibrosis, particularly the macrophage‐myofibroblast transition influenced by TGF‐β/Smad3 signaling.[12, 13] Despite these advancements, a comprehensive understanding of macrophages' multifunctional roles in renal injury and repair remains incomplete. This evidence concerns the gene TGFB1 and renal fibrosis.