The truncations of the APC protein lead to the loss of β-catenin and/or axin binding sites and prevent β-catenin degradation, resulting in abnormally high levels of cytoplasmic and nuclear β-catenin in colon tumor cells (Munemitsu et al., 1995; Faux et al., 2004). This evidence concerns the gene AXIN1 and colonic neoplasm.