In conclusion, we identify several recurrent high-level amplifications with a major impact on gene expression in MSS CRC, including the known and targetable ERBB2, but also novel amplicons such as TOX3 and ANXA11. We also propose that the epithelial/canonical subtype CMS2 has a stronger copy number-related genetic basis than subtypes more heavily influenced by gene expression signals from the tumor microenvironment. The gene discussed is TOX3; the disease is neoplasm.