Additionally, selective inhibition of HDAC1 and HDAC3, enzymes whose expression in tumors is associated with significant decreases in overall survival of human GBM patients, leads to increased temozolomide (TMZ)-induced cell death in vitro through the hyperacetylation of the NF-κB subunit p65 and inhibition of its interaction with NF-κB coactivators KAT2B and KAT3B and increased interaction with ING4, a tumor suppressor (51, 56). This evidence concerns the gene NFKB1 and glioblastoma.