Such an early ERBB2 amplification may have enabled the initiation of tumorigenesis, and the inactivation of APC and TP53 followed malignant transformation, suggesting that the role of the Wnt/β-catenin pathway in APC loss as well as the sequence of the other genomic events in CRC is largely dependent on the mutational contexts. This evidence concerns the gene ERBB2 and colorectal carcinoma.