Despite evidence that inhibition of GSK-3β causes rapid nuclear export of endogenous and exogenous AR in multiple prostate cancer cell lines, as well as confirmation that the GSK-3β inhibitors used here had the expected effect of stabilizing β-catenin levels72 (Fig. 6D), GSK-3β inhibition had no effect on the subcellular localization of wildtype or mutant AR in PC12 or HEK293 cells (Fig. 6A,B). The gene discussed is AR; the disease is prostate carcinoma.