Specifically, the current clinical molecules rely on a covalent modifier strategy that has strict specificity for the C12 residue, which is present in humans at a prevalence of only 3.4% in colorectal cancers and in 7.4% of non-small-cell lung cancer (NSCLC) cases.5 Furthermore, as clinical studies progress with G12C inhibitors, resistance mechanisms to these new drugs are being mapped, including identification of additional changes to the KRAS protein itself.6 For the remaining more prevalent KRAS mutations (e.g., G12D, G12V), significant challenges remain. This evidence concerns the gene KRAS and non-small cell lung carcinoma.