Interestingly, statins, widely used to lower cholesterol, have shown efficacy in killing KRAS mutant (KRASMUT) cells in vitro and in tumor models.5, 8–10 Statins inhibit the mevalonate pathway, necessary for KRAS prenylation, a post-translational modification required for its localization to the cell membrane where it exerts oncogenic effects.9, 11–14 By inhibiting prenylation, statins disrupt KRAS function, impeding its role in promoting tumor growth.15 This raises the question of whether statins might also achieve selective uptake specifically in KRASMUT cells. The gene discussed is KRAS; the disease is neoplasm.