Further mechanistic studies into the divergent responses following KRASG12C inhibitor treatment and transcriptional modulations controlling new KRAS synthesis in drug-induced quiescent cells will uncover new therapeutic targets and modalities to overcome adaptive resistance to current KRASG12C inhibitors.452 KRAS inhibitors often trigger a cytostatic response in cancer cells and targeting a quiescent cell state will strengthen tumor targeting and likely lead to tumor cell death to achieve durable and complete responses in cancer patients. This evidence concerns the gene KRAS and neoplasm.