We postulate that the loss of p63 relieves the inhibition of TGF-β/activin signaling via FST thereby promoting tumor epithelial cell migration and metastasis, and these processes are intertwined with cross-talk between cancer cells and other key components in the TME such as fibroblasts, as in the case of prostate cancer (105). The gene discussed is TGFB1; the disease is prostate carcinoma.