In a separate study,treatment with the XPO1 inhibitor selinexor significantly suppressed tumor growth across tenKRAS-mutant NSCLC PDX models, regardless of the specific KRAS mutation, suggesting a broaddependency of KRAS-mutant cancers on XPO1 [29].Supporting this, a genome-wide CRISPR/Cas9 screen conducted on 808 cancer cell lines (CancerDependency Map Project) identified XPO1 as a dependency in over 90% of lines, classifying itas a ‘common essential gene’ [12].Additionally, multiple studies have implicated XPO1 as a general vulnerability acrossmultiple cancer types [30–33]. This evidence concerns the gene KRAS and neoplasm.