The initiating event, we postulate, was the defective antigen loading (and its eventual display on the cell surface) because ectopic expression of CD74 restored the entire repertoire of changes to an “IRF8 WT baseline.” Of the immune perturbations that we detected in the in vivo model of IRF8-mutant B cell lymphoma, previous associations existed with NK cells depletion and Treg accumulation. This evidence concerns the gene IRF8 and B-cell non-Hodgkin lymphoma.