Kramer and colleagues suggested that induction of cancer cell apoptosis with the treatment of HDACi such as VPA is driven by hyperacetylation of Stat1 that allow its interaction with NF-kB and reduces NF-kB signaling [191], thus suppressing expression of NF-kB target genes including Bcl-XL, survivin, and Stat5. This evidence concerns the gene NFKB1 and cancer.