The concept to target KRAS synthetic lethality, premised by the notion that oncogenic KRAS signaling fuels a unique cell state, manifested by adaptation to oncogenic stress and transcriptional, translational and metabolic reprogramming, and that interfering with this KRAS-driven cell state may result in selective cytotoxicity for KRAS-mutant cancer, provides an alternative strategy for treating KRAS-driven cancers [10, 11]. The gene discussed is KRAS; the disease is cancer.