Literature data reported that p53 may drive apoptosis in tumor cells by acting both at the nuclear level, by promoting the transcription of pro-apoptotic genes, such as Bax and Bak, and at the cytoplasmic level, by directly binding to anti-apoptotic mitochondrial proteins Bcl-2 and Bcl-XL, and resulting in neutralization of their inhibitory effects. This evidence concerns the gene BAK1 and neoplasm.