Taken together with our observations that KLF5 was indispensable for tumor formation (Figs. 2a–d and 3e–h), absence or knockdown of KLF5 induces EMT (Figs. 2e and 3l, and Supplementary Figs. 2–4), downregulation of KLF5 is indispensable for TGF-β to induce EMT46, and TGF-β and Ac-KLF5 form a signaling axis to repress cell proliferation while inducing and maintaining EMT, we conclude that, at least in some cancers, the status of KLF5 loss determines whether TGF-β is a tumor suppressor or a tumor promoter. The gene discussed is KLF5; the disease is cancer.