In androgen-dependent LNCaP PCa cells, androgen treatment repressed target genes of WNT/β-catenin, whereas inhibition of AR activity enhanced WNT/β-catenin-responsive transcription; this data suggested that under the hormone-naïve condition, AR signaling could repress β-catenin/TCF-mediated transcription induced by androgen [96] (Figure 4A). The gene discussed is AR; the disease is posterior cortical atrophy.