The fact that both ATP and melatonin rescue neuronal cytotoxicity from VDAC-associated mitochondrial dysfunction may offer an explanation as to why p53 is found to be elevated in AD patients [728], and why tau increases wild-type p53 expression through the modulation of MDM2 [788,789,835], the E3 ubiquitin ligase which is also used by melatonin to activate p53 [836]. The gene discussed is TP53; the disease is Alzheimer disease.