Thus, to explain the variable responses of EGFR/KRAS co-mutated patients, the authors inferred that KRAS-induced intrinsic resistance may ensue only when the relative AF of KRAS-mutants is sufficiently high to counteract the effect of EGFR-TKIs on cancer cells [53], a concept that in principle may be applied to other resistance-associated co-mutations. The gene discussed is KRAS; the disease is cancer.