Activated TβRI and JNK differentially phosphorylates the mediator Smad3 to become pSmad3C (Ser-423/425) and pSmad3L (Ser-213) and then transmits tumor-suppressive or oncogenic TGF-β signaling, respectively, by mediating distinct transcriptional responses [24, 25]. The gene discussed is TGFBR1; the disease is neoplasm.