Some studies describe a more favorable clinical outcome in patients with CRC with a KRAS A146-mutated tumor upon anti-EGFR treatment compared with patients with tumors carrying another KRAS mutation.54-57 Other studies show that tumors with a KRAS A146 mutation, like other KRAS mutations, are responsible for anti-EGFR resistance.58-61In this study, the homogenous population of initially unresectable liver-only metastatic CRC patients all receiving the same treatment regimen allowed for an unbiased comparison of the clinical features of patients harboring different KRAS tumor mutations. This evidence concerns the gene EGFR and neoplasm.