NLRP3 deficiency prevents the decrease in tyrosine hydroxylase (TH) expression, loss of the dopaminergic neurons in the substantia nigra, and striatal dopamine production as well as the formation of α-synuclein in chronic and subacute MPTP-treated mice (33, 34), indicating that targeting NLRP3, or the crucial molecules of the inflammasome, caspase-1 and IL-1β, may shed light on PD treatment. This evidence concerns the gene TH and Parkinson disease.