Multiple explanations for the effects on atherosclerosis observed in Fcgr2b−/− mice are possible since several anti-inflammatory pathways (increased Treg, increased Th2 cells, an M1 to M2 switch in macrophages, cytokine production by macrophages) and pathogenic pathways (autoantibodies, increased CCL2, increased T cell infiltration, more IL-17 and IL-23, increased FcγRIII on macrophages) are implicated across the various studies. The gene discussed is IL17A; the disease is atherosclerosis.