Chronic-IFN-γ-treatment of tumour cells induced STAT1-associated epigenomic changes, promoting IFN-γ-independent expression of ISGs including ligands for multiple TCIRs, such as TNF receptor superfamily member 14 (TNFRSF-14) and MHC-II, that conferred resistance to ICBT in preclinical models [74]. The gene discussed is STAT1; the disease is neoplasm.