Abstract
Kirsten rat sarcoma viral oncogene (KRAS) among the most common oncogenic driver mutations in non–small cell lung cancer (NSCLC).1 RAS is activated by binding to guanosine triphosphate (GTP), which subsequently activates several downstream pathways, including RAF, PI3Ks, RALGDS, and phospholipase C.2 Although there are several known KRAS mutations, the most common KRAS mutations lead to impaired GTPase activity and permanent activation of RAS signaling. Unfortunately, despite numerous efforts, there have been no effective targeted therapies for KRAS that have been developed to date.
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