We propose a circuitry wherein the poor antigen presentation by IRF8-mutant lymphomas (due to deregulated CD74/antigen loading) blunts the activation and differentiation of naïve CD4+ T cells toward the TH1 phenotype, decreasing the secretion of proinflammatory cytokines such as IFN-γ, which in turn limits the recruitment of NK, NKT, and pDC cells, all themselves significant sources of IFN-γ and tumor necrosis factor α (60, 61), thus further suppressing the beneficial inflammatory profile of the TME. This evidence concerns the gene IFNG and lymphoma.