In 2013, Ostrem et al. (7) reported the development of a covalent inhibitor that was able to lock KRAS into its inactive guanosine diphosphate (GDP)–bound state by binding to the cysteine resulting from the G12C mutation, present in 40% of KRAS-mutant NSCLC patients. This evidence concerns the gene KRAS and non-small cell lung carcinoma.