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However, further in-depth studies will be required

MLKL is known to be a substrate of RIPK3, which can induce the formation of an NLRP3/caspase-1 inflammasome, as well as promote RIPK3-dependent caspase-8 activation, finally resulting in caspase-8 cleavage of pro-IL-1, and induce both inflammation and necroptotic cell death

Lancet 366 , 10591062 (2005)

Human cells use these same mechanisms [7]

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