The failure of polarity proteins to localize correctly to the membrane during EMT relieves the sequestration of Smads, e.g. the inhibitory interaction between the crumbs polarity complex and Smad3 that is mediated by YAP and TAZ, and promotes TGF-β signaling, which, in turn, stabilizes the EMT phenotype and eventually enables tumor cells to evade anoikis [32, 33]. The gene discussed is TGFB1; the disease is neoplasm.