Turnover of β-catenin protein is tightly controlled by the destruction complex (APC/Axin/CKI/GSK3/β-TRCP) (Hart et al., 1999), in which mutation of either APC or AXIN, as well as inactivation of GSK3 can impair the degradation of β-catenin (Sparks et al., 1998; Rubinfeld et al., 1993), in turn these alterations directly link this pathway to hereditary diseases, including colon cancer (Morin et al., 1997; Lammi et al., 2004). Here, AXIN1 is linked to colonic neoplasm.