The common tumor-initiating event in human colon cancers is hyperactive WNT-TCF signaling, usually through mutation of the negative regulator adenomatous polyposis coli (APC) and the consequent constitutive activation of β-CATENIN, which then interacts with nuclear TCF/LEF factors to regulate target gene transcription (Morin et al, 1997; MacDonald et al, 2009; Valenta et al, 2012). The gene discussed is APC; the disease is neoplasm.