Interestingly, a cross-talk between AR and Akt has been recently demonstrated in prostate cancer, whereby inhibition of Akt in cells expressing high levels of p-Akt resulted in decreased AR protein levels, overexpression of Akt resulted in increased levels of AR protein, while inhibition of low levels of endogenous Akt kinase activity did not affect AR protein levels [38]. The gene discussed is AR; the disease is prostate carcinoma.