Given the role of β-catenin as an AR co-activator [31,32], our data further showed that elevated β-catenin promotes AR-mediated transcription and cell growth in E-cadherin deleted prostate cancer cells, elucidating the molecular mechanisms for loss or reduction of E-cadherin in inducing oncogenic transformation and PIN development. The gene discussed is CDH1; the disease is prostate intraepithelial neoplasia.