Finally, Selinexor-induced MGMT expression and pCREB<sup>S133</sup> were blocked by the protein kinase A inhibitor H89, suggesting a role for PKA-CREB signaling in this process.<h4>Conclusions</h4>This study demonstrates XPO1 as a mediator TMZ resistance in MGMT-methylated GBM cells, and that MGMT expression status is a potential determinant of sensitivity to Selinexor/TMZ treatment in GBM cells. This evidence concerns the gene CREB1 and glioblastoma.