Additionally, knockdown of HDAC2 did not abrogate but further enhanced the pro-apoptotic effect of VPA+TMZ co-treatment in either p53 wild-type GBM cell line, as inferred from the increased PARP cleavage and caspase 9 and caspase 3 activation (Figures 4A, B). This evidence concerns the gene HDAC2 and glioblastoma.