A previous study found that global or CD4+ T cell-specific dopamine 2 receptor (DRD2) deficiency could exacerbate MPTP-induced dopaminergic neurodegeneration and CD4+ T-cell depolarization towards pro-inflammatory Th17 phenotypes, indicating that DRD2 expressed on CD4+ T cells is protective against neuroinflammation and developing a therapeutic strategy of stimulating DRD2 may be promising for amelioration of Th17-inflammatory response in PD [123]. The gene discussed is DRD2; the disease is neurodegenerative disease.