Paradoxically, STAT1 has also been shown to inhibit these phenotypes by enhancing transcription of CXCL9, CXCL10, and CXCL11, leading to longer overall survival and progression-free survival in patients, and reduction of ascites formation and tumor burden in ID8 OvCa murine models of disease [65,66]. The gene discussed is STAT1; the disease is neoplasm.