In KRAS-mutant cancer cells, published evidence reveals a dependency on XPO1-mediated nuclear transformation for growth and survival.259 Similarly, evidence from KRAS-mutant lung cancer patient-derived xenografts revealed the antitumor efficacy of the XPO1 inhibitor selinexor.260 Moreover, XPO1 expression is linked to resistance to various therapies, making it a promising target for novel cancer therapies.261–263. This evidence concerns the gene KRAS and cancer.