TP53 and neoplasm: The silencing of cell cycle inhibitors like CDKN2A in the TP53 pathway, for example promotes cell proliferation in HCC while silencing of the APC tumor suppressor promotes β-catenin expression and the development of EMT (152, 153) HBx (EZH2) downregulated miR-101 can also fail to modulate MCL-1, a key anti-apoptotic member of the BCL-2 family, thus promoting survival in HCC cells as a result of suppressing caspase driven apoptosis (152, 154).