The current publication from Singha et al. [9] extends these findings, showing that through coordinate regulation of the canonical and noncanonical signaling pathways (Fig. 1), TMEPAI acts to suppress the cytostatic consequences of the canonical pathway while potentiating the proliferative effects of the noncanonical pathway, thus dramatically changing the outcome of TGF-β exposure from tumor inhibition into growth promotion. The gene discussed is TGFB1; the disease is neoplasm.