The disability of BCL-2/BCL-xL to suppress the BAX/BAK pro-apoptotic function in the NPC cells occurs due to the initiation of p-CDK1 (Thr 161)–cyclin B1-induced BCL-2 (Thr 69 and Ser 87)/BCL-xL (Ser 62) phosphorylation [30]. This evidence concerns the gene BAK1 and nasopharyngeal carcinoma.