In the colorectal carcinoma model system [tamoxifen-inducible Cre to activate Kras with inactivation of Apc (AK) ± altered Trp53 (AKP) in epithelial cells of the colorectum (via the Cdx2 promoter); ref. 45] evaluated by MiMouse, oncogenic mutations and high-level CNAs were also exceptionally rare, although we identified prioritized Smad4 and Pik3ca mutations and Pik3ca and Myc amplifications, with these being among the most frequent mutations/amplifications in human microsatellite-stable colorectal carcinoma (beyond those genetically altered in our mouse models; refs. 46–48). The gene discussed is MYC; the disease is colorectal carcinoma.