Sodium Butyrate (Butanoic acid sodium salt) is a histone deacetylase (HDAC) inhibitor, with anti-tumor effects in several cancers. In Vitro: Sodium Butyrate induces morphological changes, inhibits cell proliferation and impairs cell viability in NPC cells. Sodium Butyrate (1, 5, 10 mM) is cytotoxic to NPC cells, inducing a dose- and time-dependent decrease in cell viability, in both 5-8F and 6-10B cells. Sodium Butyrate induces nasopharyngeal carcinoma cell apoptosis by activating the mitochondrial apoptotic axis. Moreover, SOCE inhibition and disruption of the CRAC channel can attenuate the apoptosis induced by Sodium Butyrate^[1]. Sodium butyrate significantly decreases cell viability, accompanied by reduced levels of p-mTOR and PCNA protein. Sodium butyrate, in a dose-dependent manner, induces cell cycle arrest in G0/G1 phase and reduces the numbers of cells in S phase. In addition, relative expression of p21, p27, and pro-apoptosis bak genes, and protein levels of p21Waf1/Cip1, p27Kip1, cyclinD3, CDK4, and Cleave-caspase3 are increased by higher concentrations of sodium butyrate (1, 5, 10 mM), and the levels of cyclinD1 and CDK6 are reduced by 5 and 10 mM butyrate^[3]. In Vivo: Sodium Butyrate (300 mg/kg, s.c.) administration immediately after HI provided almost complete neuroprotection in comparison with non-treated animals. Sodium butyrate administration results in an increased number of microglial cells to 150% of vehicle-treated animals in the ipsilateral side. Sodium butyrate promotes the polarization of microglia from M1- to M2-like phenotype after neonatal hypoxia-ischemia^[2]. Sodium butyrate (300 mg/kg, s.c.) in combination with AK-7 (20 mg/kg, i.p.) significantly alleviates this reduction of the time spent exploring new objects, ameliorates the reduction of the number of Ki67-positive cells and DCX-immunoreactive neuroblasts in the dentate gyrus of the mice. In addition, sodium butyrate reverses SIRT2-related age phenotypes^[4].