Indeed, NLRP3 was shown to be an important mediator of neuroinflammatory responses in AD (Halle et al., 2008; Heneka et al., 2013) and intra-hippocampal injection of Aβ in mice increases the amount of IL-1β produced, only in the presence of an active P2X7 (Rampe et al., 2004; Sanz et al., 2009). The gene discussed is IL1B; the disease is Alzheimer disease.