In this work, we have deciphered the mechanisms of AR variants-induced N-cadherin differential expression, showing that N-cadherin upregulation in prostate cancer cells appears to result from the binding of AR variants to AREs in intron 1 of the CDH2 gene followed by histone H4 acetylation, but also from a decrease of endogenous AR-FL. This evidence concerns the gene AR and Familial prostate cancer.