The combination therapy of selinexor and PD-1/PD-L1 blockade exerted superior anti-tumor activity than either therapy alone in animal models.5 Moreover, preclinical studies demonstrated that EBV SM protein’s nuclear exportin is mediated by XPO1 and XPO1 inhibitor could suppress the replication of EBV, a favorable signal for the control of EBV-driven NKTCL.6,7. The gene discussed is CD274; the disease is neoplasm.