Moreover, Btk is central in control of the Toll-like receptor (TLR)-induced IL-10 expression by B cells, and is an active part of the NLRP3 inflammasome, a multimeric protein complex that triggers the release of proinflammatory cytokines, such as IL-1β and IL-18, in many inflammatory conditions, including Alzheimer’s disease, diabetes, and infections (55), and lack of Btk can lead to a compromised BCR-induced proliferation and survival. This evidence concerns the gene BTK and early-onset autosomal dominant Alzheimer disease.