TNFα, IL-1β, IL-6, and IL-18 have been reported to be upregulated in AD brains and further progress AD pathology by releasing Aβ peptides and attenuating Aβ clearance, thus increasing the opportunity for plaque formation, and by inducing tau hyperphosphorylation and NFT formation through altered p38 MAPK/GSK3 signalling [48,72,73,74,75]. The gene discussed is IL18; the disease is Alzheimer disease.