By far, major EMT-associated therapies aim at reverting or preventing EMT through targeting different aspects of this process, involving modulation of upstream pathways such as WNT, NOTCH, and TGF-β signaling (77), manipulation of stromal cells in the microenvironment such as tumor-associated macrophages, neutrophils and fibroblasts, employment of EMT-repressing miRNAs (78, 79), and direct inhibition of EMT-TFs via CRISPR–Cas9 (18, 80). Here, TGFB1 is linked to neoplasm.