The defective activation of CD4 (but not CD8) T cells by IRF8-mutant B cell lymphomas, together with the well-recognized role of MHCII deficiency in DLBCL biology (56), suggested that IRF8 variants may deregulate genes and processes that are involved in antigen loading/processing and/or presentation. This evidence concerns the gene CD8A and B-cell non-Hodgkin lymphoma.