We have established that the hyperactivation of Wnt signaling activity in NaB-treated CRC cells results from increased levels of Ser-37/Thr-41-dephosphorylated (active) beta-catenin, augmented formation of BCT complexes, as well as enhanced BCT complex-DNA binding [1,2]. The gene discussed is PCYT1B; the disease is colorectal carcinoma.