Mechanistically, they demonstrated melatonin inhibited hrTNFα-induced activation of NFκB [54], a transcription factor that may promote prostate cancer viability via upregulation of c-myc, cyclin D1, and IL-6, and more relevantly, activation of anti-apoptotic genes, such as B-cell lymphoma 2 apoptosis regulator (Bcl-2) [119]. Here, BCL2 is linked to prostate cancer.