Together, these studies, along with our findings of altered FcγRIIB expression on B cells in GPA and the strong association of FcγRIIB expression on several B cells including CD38−CD24−/lowCD19−/+CD20−/+ anergic naive, naive/unswitched memory, and IgA+CD38−/+CD27−/+CD86−/low switched activated memory with disease activity, support a potential role for FcγRIIB in GPA pathogenesis. This evidence concerns the gene CD27 and granulomatosis with polyangiitis.