Given that FcγRIIb was initially reported as a hematopoietic receptor which is mainly expressed in B cells, macrophages, and neutrophils (Nimmerjahn and Ravetch, 2008), our data using 3xTg-AD/FcγRIIb KO mice raised a possibility that FcγRIIb in non-neuronal cells might contribute to APP/Aβ-induced tau pathologies via neuroinflammatory function. The gene discussed is APP; the disease is Alzheimer disease.