Having uncovered a role for BTK in activating microglial PLCγ2, an AD-associated risk factor (Sims et al. 2017), and in regulating microglial phagocytosis including the uptake of synaptic structures, we next wished to investigate whether BTK is involved in the pathophysiology of AD, a neurodegenerative disease in which microglia have been proposed to mediate synaptic loss (Hong and Stevens 2016). The gene discussed is BTK; the disease is Alzheimer disease.