Elucidating the mechanisms by which tumor cells hijack the IFN-γ pathway to suppress antitumor response including MHC-I and CXCL9/10/11expression, while preferentially enhancing the expression of immunosuppressive molecules such as PD-L1 and IDO1, would shed light on the conflicting identify of IFN-γ in tumor progression, along with providing therapeutic targets to improve current immunotherapies. The gene discussed is CD274; the disease is neoplasm.