In line with our data demonstrating the relevance of IDO activity for the suppression of anti-tumor immune responses and the relevance of STAT3 activation for constitutive IDO activity in human cancer, interference with constitutive STAT3 signaling in IDO-positive cancer cells using either the phospho-STAT3 inhibitors AG490 and JSI-124 or the histone acetyltransferase inhibitor HATI resulted in enhanced proliferation of allogeneic T-cells in SKOV-3/MLR cocultures (Fig 2H). The gene discussed is STAT3; the disease is cancer.