Moreover, the fact that melatonin modulates caspase activity [160], thereby preventing apoptosis [215, 216], suggests that the hormone could lessen the cell cycle re-entry-induced and caspase-dependent apoptosis taking place in AD [22], while the ability of melatonin to inhibit the ubiquitination-dependent proteasome pathway may provide a promising track in the quest to treat neurodegenerative disorders like AD [217] when considering that the ubiquitin-proteasome system (UPS) is involved in the cell cycle progression and is deregulated in AD [218]. This evidence concerns the gene UBC and Alzheimer disease.