In anti-tumor immunity, chronic persistent type II interferon signaling enables STAT1 tumor-related epigenetic changes, resulting in increased expression of interferon-stimulated genes and inhibitory receptors (TCIRs) on multiple T cells, including LGALS9 (Galectin-9), MHCII ligands, and immune inhibitory checkpoints, including TIM3 and LAG3. The gene discussed is STAT1; the disease is neoplasm.