In solid cancer, resistance to ICIs is related to a non-inflamed TME, where effector T cells are physically excluded, or deprived of normal anti-tumor function via several kinds of mechanisms, including defects in neoantigen presentation, defective IFN-γ signaling pathway, upregulation of other inhibitory checkpoint molecules, and immunosuppressive metabolites and cell populations in the TME (Lei et al., 2020; Schoenfeld and Hellmann, 2020). The gene discussed is IFNG; the disease is neoplasm.