Since each cancer phenotype features a different ratio of oncogenic KRAS subtypes, the authors postulated that this allosteric inhibition will not be limited to certain cancer subtypes as it unexclusively targets wild-type and mutant (KRASG12C/D and KRASQ61H) GTP-bound KRAS subtypes and can be used across a range of tumor types as a first-line therapy. This evidence concerns the gene KRAS and neoplasm.