While canonical WNT signaling mediates cellular β-catenin levels, the level of active β-catenin (unphosphorylated at residues Ser37 and Thr41) in melanoma, breast and prostate cancer cells is reported to be regulated by the PI3K-AKT-mTOR cascade, in a process that is dependent on PP2A activity [335]. The gene discussed is AKT1; the disease is prostate cancer.