Anti–epidermal growth factor receptor (EGFR) monoclonal antibodies plus cytotoxic drugs are the treatment cornerstone for RAS wild-type (WT) metastatic colorectal cancer (MCRC).1,2 Despite initial efficacy, acquired resistance mechanisms, including KRAS or NRAS alterations,3,4,5 are associated with treatment failure in all patients.3,4 Whereas the majority of RAS WT cancer cells are killed by chemotherapy plus cetuximab or panitumumab, a genetic selection of RAS mutant cancer cells occurs with tumor progression. This evidence concerns the gene KRAS and cancer.