Our recent work [21] reveals that high levels of Cx43 in MGMT-deficient GBM cell lines and primary patient samples correlate with poor responses to TMZ and that αCT1, a clinically-tested therapeutic peptide that comprises the Cx43 carboxyl terminus (CT) and an antennapedia cell-penetrating sequence [22], antagonizes TMZ resistance. This evidence concerns the gene TRAF3IP2 and glioblastoma.