Concordantly, we find that IRF8 mutations in primary human DLBCLs are mutually exclusive with mutations in genes directly associated with antigen presentation including CIITA, a direct IRF8 target and master regulator of de novo transcription of MHCII complex genes (33–35), as well as HLA-DMB and CD74. In IRF8-mutant lymphoma models, consistent downmodulation of CD74 and HLA-DM significantly deregulated antigen presentation in an MHCII but not MHCI context (34). The gene discussed is HLA-DMA; the disease is lymphoma.