It has been reported that the primary mechanism underlying XPO1i sensitivity ofKRAS-mutant cancer cells is intolerance to nuclear IκBα accumulation, withconsequent inhibition of NF-κB signaling [13].We have earlier demonstrated that the efficacy of XPO1i selinexor and KRASG12Ci combinationscan be mechanistically attributed to the downregulation of NF-κB driven cell survivalsignaling, as well as induction of cell cycle arrest by reducing CDK4 expression andincreasing the nuclear accumulation of tumor suppressor protein RB1 [14]. The gene discussed is NFKB1; the disease is cancer.