The inhibition of HDAC6 results in activated mismatch repair (MMR) protein via MutS homolog 6 (MSH6) stabilization, as well as decreased levels of the epidermal growth factor receptor (EGFR), mutp53, O6-methylguanine-DNA methyltransferase (MGMT), and MDM2 in GBM cells, resulting in increased apoptosis when combined with TMZ treatment (Table 1) [131]. The gene discussed is HDAC6; the disease is glioblastoma.