TGFB1 and neoplasm: Their reciprocal mechanisms in the EMT-related process are demonstrated as follows [25, 27, 28]: GRHL2 suppresses EMT and restores sensitivity to anoikis by repressing ZEB1 expression; Combination of TGF-β and Wnt activation represses GRHL2 expression by direct interaction of ZEB1 with the GRHL2 promoter, inducing EMT; Reciprocal feedback loop between GRHL2 and ZEB1 controls epithelial versus mesenchymal phenotypes and EMT-driven tumor progression; GRHL2 is the main gatekeeper of EMT in EOC via miR-200-ZEB1, and their axis forms the core of EMT signaling.