The observed increase in Wnt ligand expression in prostate cancer may augment Wnt signaling and can occur via multiple mechanisms, including AR- or FOXB2-mediated transcriptional regulation of Wnt genes [67,144,145], as well as post-translational events such as N-glycosylation and acylation via palmitoylation that are required for Wnt ligand folding and/or secretion (reviewed in [146]). This evidence concerns the gene AR and prostate carcinoma.