But we can also think the opposite: that our results would even be valid for mutant EGFR glioblastomas, as it has been shown that HDAC6-selective inhibitors block activation of the EGFR and p53 pathways by increasing the levels of MSH2 and MSH6, key DNA mismatch repair proteins; by decreasing MGMT expression; and by increasing temozolomide sensitivity and efficiently inducing apoptosis in temozolomide-resistant glioblastoma cells [69]. Here, MSH2 is linked to glioblastoma.