MLKL and Alzheimer disease: Extensive research has shown thatRIPK1/RIPK3, as serine/threonine-protein kinases, can autophosphorylate themselves and form a RIPK1/RIPK3 complex (necrosome) to recruit and induce the phosphorylation of MLKL at ser358 (p-MLKL) and form RIPK3-MLKL oligomers, which subsequently activate cell necroptosis to induce membrane rupture and cell death and thus play an important role in AD pathogenesis [20, 35, 52–55].