Abstract
Although oncogenic driver mutations in RAS occur in 20% of cancers, heterogeneity in the biologic outputs of different RAS mutants has hampered efforts to develop effective treatments for RAS-mutated cancers. In this issue of Science Signaling, Huynh et al. show that even among KRAS(Q61) mutants, the specific amino acid that is substituted substantially affects mutant KRAS biologic activity and oncogenicity.