Clec7a was highly expressed in the substantia nigra (SN), striatumand reactive microglia of rats in a PD model. Knockdown of Clec7aimproved motor symptoms, protected dopaminergic neurons and reducedlevels of TNF-α, IL-1β, IL-6, IL-18 and IFN-γ inthe SN and decreased microglial pro-inflammatory polarization. Ina cell model of PD, Clec7a overexpression increased iNOS+ cells, whilegene knockdown reversed this effect and reduced SN levels of TNF-α,IL-1β, IL-18 and IL-6. This evidence concerns the gene IFNG and Parkinson disease.