Information about tumor RAS status was not available for P1, but the metastatic tumor of P2 was tested to be RAS-wild-type before chemotherapy, suggesting that the low-frequency KRAS mutation detected in P2’s plasma ctDNA almost 6 years after completion of courses of anti-EGFR (cetuximab) + FOLFIRI and anti-VEGF (bevacizumab) + FOLFIRI was a mechanism of acquired resistance. This evidence concerns the gene KRAS and neoplasm.