Alisol B binding to EIF2AK2 can inhibit its activation, effectively inhibiting Aβ accumulation and the resulting neuroinflammation; interrupting the cycle of EIF2AK2 activation, activating BACE1 and further causing Aβ accumulation; and simultaneously inhibiting Tau phosphorylation, preventing the depolymerization of neuronal microtubule cytoskeleton and the formation of NFTs, effectively controlling AD progression (Supplementary Figure S2; Figures 4, 6). Here, EIF2AK2 is linked to Alzheimer disease.