Analysis of baseline tumor mutations showed that a higher proportion of patients with TP53 mutation acquired MET amplification following treatment with Enco+Cetux±Bini than those with wild-type TP53 (odds ratio = 4.3; P = 0.006) (Fig. 6d); this difference between the TP53 mutant and wild-type subgroups was consistent when considering the acquisition of any putative resistance amplification (that is, MET, KRAS, BRAF, IGF1R; odds ratio = 4.2; P = 0.0006) (Supplementary Fig. 10). This evidence concerns the gene KRAS and neoplasm.