In this regard, Salimu et al. [108] showed that prostate cancer-derived ExVs activated the expression of CD73, an ecto-5-nucleotidase responsible for the hydrolysis of AMP into adenosine, on DCs so resulting in an ATP-dependent inhibition of TNFα- and IL-12-production and suppression of DC function via ExV prostaglandin E2. The gene discussed is NT5E; the disease is Familial prostate cancer.