In the molecular mechanism of the apoptotic celldeath program,a shift in Bax/Bcl-2 expression ratio at the transcriptional levelinitiates apoptosis by activating Caspase-3, as was reported in varioustumors.15 In the early stage of the apoptosismechanism, activation of the p53 tumor suppressor leads to the expressionof pro-apoptotic mediators including the Bax/caspase-3 and the inhibitionof Bcl-xL/Bcl-2. This evidence concerns the gene BAX and neoplasm.