The oral administration of NAM, a non-selective SIRT1 and SIRT2 inhibitor but with lower IC50 to SIRT1 (Table 1), to 3xTg-AD mice, restored a cognitive deficit in these mice by reducing phosphorylated tau, and improved autophagy-lysosome procession in the hippocampus and cerebral cortex (Liu et al., 2013). The gene discussed is SIRT1; the disease is Alzheimer disease.