On plasma cells and B-1 cells, FcγRIIb has a direct proapoptotic influence that is continuously counteracted by survival factors such as BAFF (B cell–activating factor) of the TNF (tumor necrosis factor) family.13,14 FcγRIIb genetic mutations are associated with SLE and also with total IgG levels in humans, suggesting an important role for FcγRIIb in B cell–dependent regulation of disease.15,16 Investigations into the role of FcγRIIb in atherosclerosis have to date focused on Fcgr2b−/− mice, with conflicting reports. Here, TNF is linked to systemic lupus erythematosus.