Microglia activation can have a neurotoxic role in AD through activation of the complement system (e.g., C1q, C3) and the inflammasome, release of pro-inflammatory mediators [e.g., interleukin-1 (IL-1), IL-6 and tumor necrosis factor α (TNFα)] and leading to synaptic loss, mitogen-activated protein kinase (MAPK) activation and subsequent NFTs formation (Griffin et al., 2006; Heneka et al., 2013; Dursun et al., 2015; Wang et al., 2015; Hong et al., 2016; Fonseca et al., 2017; Liddelow et al., 2017). The gene discussed is IL1B; the disease is Alzheimer disease.