Further evidence for a critical role for the NLRP3 inflammasome mechanism in PD is that pharmacological inhibition of its activation or knockdown of either NLRP3 or caspase-1 gene expression protected mice in various in vivo parkinsonism models against both dopaminergic neurodegeneration and the spreading of α-syn pathology [12, 30–32]. This evidence concerns the gene CASP1 and Parkinson disease.