Salermide (11, Table 2), which resulted from the med-chem optimization of sirtinol, is a moderate SIRT1/2i that induces cancer-specific pro-apoptotic effects on different tumor cells (mainly MOLT4, KG1A, SW480, and Raji) through reactivation of pro-apoptotic genes (CASP8, TNF, TNFRSF10B, and PUMA) previously repressed by SIRT1-mediated H4K16ac deacetylation [65] and through the upregulation of DR5 [66]. This evidence concerns the gene SIRT1 and neoplasm.