Srivastava et al. used a benzamide histone deacetylase inhibitor (MS-275 also called entinostat) to target histone deacetylase (HDAC) 1/3, leading to an increase in the apoptosis-inducing potential of TRAIL in different cancer cell lines in vitro.113 This treatment enabled to sensitise TRAIL-resistant cancer cells, a phenomenon also observed in vivo (breast cancer xenografts in nude mice) where MS-275 inhibits EMT, decreases NF-κB pathway activation and finally increased DR4/DR5 receptor and pro-apoptotic protein expression. This evidence concerns the gene TNFSF10 and breast cancer.