KD of HDAC2 upregulates miR-449 and downregulates c-MET expression, which inhibits tumour growth; KD of HDAC2 activates p53 and Bax but suppress Bcl-2 to induce apoptosis; KD induces expression of p21 and suppresses cyclin E2, cyclin D1, and CDK2 expression to induce cell-cycle arrest; KD HDAC2 increases expression of NOXA, which sensitizes tumour cells towards etoposide-induced apoptosis (94, 96, 97). The gene discussed is BCL2; the disease is neoplasm.