All of these molecules have been implicated in impaired immune response against ovarian carcinomas, either by direct TGF-β1-mediated effects [9, 38, 39], or by indirect effects resulting from the breakdown of ATP into adenosine by CD73, which promotes the immunosuppression of T cytotoxic and NK lymphocytes [9, 37]. The gene discussed is TGFB1; the disease is ovarian carcinoma.