To summarize, (1) reduction of IL-33 production per se, (2) increased concentrations of the sST2 decoy receptor, and (3) an impairment of the ability of IL-33 to induce NF-kB nuclear translocation are different mechanism that can explain the proinflammatory role played by IL-33 in AD and MCI. The gene discussed is IL33; the disease is Alzheimer disease.