In NSCLC, objective response rates from early-phase studies with KRASG12C inhibitors were lower than agents targeting EGFR-activating mutations or ALK-RET fusions.29,30 This suggests greater biological diversity and oncogenic pathway redundancy in KRASG12C-mutant tumors compared with tumors driven by other oncogenes. This evidence concerns the gene EGFR and non-small cell lung carcinoma.