A recent study by Tripathi et al. has implicated nuclear protein export as animportant non-canonical pro-oncogenic function of RAS and reported that mutant KRASinhibition in lung cancer phenocopies XPO1 inhibition, but the effect of KRAS inhibition onXPO1-dependent activity is independent of canonical KRAS downstream pathways RAF/MEK andPI3K/AKT. This evidence concerns the gene AKT1 and lung cancer.