In the absence of TβR‐V in late‐stage cancer, TGF‐β induces EMT (epithelial–mesenchymal transition), autoinduction, and increased invasiveness by stimulating TβR‐I‐activated or TβR‐I‐mediated non‐Smad signaling pathways37, 38, 39, 40 as well as canonical Smad signaling (TβR‐I/TβR‐II/Smad2/3/4 signaling).13 Here, TGFBR2 is linked to cancer.