Indeed, in several types of cancer, a TGF‐β1‐rich tumor microenvironment is maintained by some immune cells, and Tregs, and macrophages, and platelets can serve as the primary TGF‐β1 producers.[37] Consistently, we observed an elevated expression of TGF‐β1 in CD45+ leucocytes and F4/80+ macrophages after Smad4 deletion during colitis, although it could be a secondary response to the injured epithelial after DSS treatment. The gene discussed is TGFB1; the disease is colitis.