Inhibition of RIPK1 not only genetically rescued the postnatal lethality of Nek1Kat2J/Kat2J mice by inhibiting BBB damage, but also reduced neuroinflammation and the accumulation of misfolded proteins such as α-synuclein, suggesting that the activation of RIPK1-mediated inflammation might also contribute to the disruption of cellular homeostasis which in turn promotes the accumulation of α-synuclein in the pathogenesis of Parkinson’s diseases and the cognitive dysfunction in Alzheimer’s disease66–68. This evidence concerns the gene RIPK1 and Parkinson disease.