TGF‐β stimulates the conversion of endothelial cells into CAFs, while bone morphogenic protein 7 (BMP7) maintains the endothelial fate,15 indicating that antiangiogenic treatment of tumours, such as TGF‐β inhibitors or BMP7 agonists, may function as potential targets for decreasing activated fibroblasts. This evidence concerns the gene TGFB1 and neoplasm.