BTK and Alzheimer disease: According to GWAS and corresponding research in vitro and in vivo, PLCγ2 might be an important player influencing the formation of Aβ plaques and P-tau, the main hallmarks in AD pathophysiology, and regulating the pathways associated with neuroinflammation and AD-related effector proteins (e.g., TREM2, TLR4, BTK, and CSF1R).