This role seems to involve the activation of canonical Wnt3a pathway as suggested by the association between AurkA overexpression and nuclear/cytoplasmic localization of β-catenin (Pvalue = 0.00001) found in 89 breast cancer primary tumors (Fig. 1A) as well as the association between AurkA expression and β-catenin stabilization found in our experimental model (western blot in Fig. 3A,B). This evidence concerns the gene AURKA and breast cancer.