However, our present study showed that the cytoplasmic accumulation and nuclear localization of β-catenin induced by the overexpressed AQP1 in breast cancer did not activate the Wnt downstream target genes such as C-Myc, CCND1, CD44, and MMP2. We also demonstrated that AQP1 and GSK3β could competitively interact with the 12 armadillo repeats of β-catenin in the inhibition of the ubiquitin-proteasome degradation pathway of β-catenin. The gene discussed is CD44; the disease is breast carcinoma.