Increasing evidence suggests that immune mechanisms contribute to the pathogenesis of AD including reactive microgliosis in postmortem samples, increased microglial activation marker, translocator protein (TSPO), binding on positron emission tomography (PET), [6] and increased pro-inflammatory cytokines such as interleukin (IL)-6, IL-1β, TNF, and IFN-γ in the cerebrospinal fluid and serum [7–11]. The gene discussed is TSPO; the disease is Alzheimer disease.