Among the secreted cytokines, IFN-γ receptors 1 and 2 induce JAK/STAT-mediated IRF-1 activation, increasing the expression of PD-L1 in regulatory T cells, tumor-associated macrophages, and myeloid-derived suppressor cells within the tumor microenvironment [13]; as a result, the immunosuppressive microenvironment in a high state is maintained, and the aggressiveness of the tumor cell is accelerated. The gene discussed is IRF1; the disease is neoplasm.