This was accompanied by enhanced expression of the apoptosis-related proteins cleaved caspase-3 and Bax and suppressed expression of pro-caspase 3 and Bcl-2 within the tumor, indicating that the observed antitumor efficacy is mediated through the induction of apoptosis, likely triggered by cellular stress induced by co-treatment with VPA and AA. This evidence concerns the gene CASP3 and neoplasm.