Trotta et al. 17 recently reported of suppressed CD16-mediated IFN-γ production of NK cells by TGF-β1 via Smad3–T-bet-dependent pathway, so we compared the relative impact of E4BP4 versus T-bet on Smad3-mediated NK cell antitumour activities by adoptive transfer of the Smad3−/− NK cells with or without knockdown of E4BP4 (Nfil3) or T-bet into the B16F10 tumour-bearing NOD/SCID mice. The gene discussed is NFIL3; the disease is neoplasm.