The significance of focal amplification as a mechanism of oncogenic activation during EAC transformation30,31 is further supported by the observations of recurrent amplifications of EAC oncogenes, including ERBB2 on 17q (5/15 patients) (Supplementary Fig. 9A, B) and GATA6 on 18q (4/15 patients), distinct amplifications in different cancers from the same patient (Supplementary Fig. 9C, D), and sporadic oncogene amplifications that are exclusive to cancer lesions but not their precursors, including IGF1R (patient 3), MET (patient 4, Fig. 6C), and KRAS (patient 10 and Supplementary Fig. 9E). This evidence concerns the gene KRAS and cancer.