This conception is corroborated by (i) alleviation of spatial memory deficits together with modulation of the histopathological changes, (ii) decrement of AD hallmarks (p-Tau and Aβ plaques), (iii) suppression of the necroptotic p-RIPK1/p-RIPK3/p-MLKL signaling pathway, and (iv) mitigation of neuroinflammation as well as neuronal death. The gene discussed is MLKL; the disease is Alzheimer disease.