Importantly, in vivo studies in PD models have demonstrated that the abnormally increased secretion of TNF-α and IFN-γ perpetuates microglial and astroglial neuroinflammation by sustaining the TNF-α/janus kinase/STAT- and IFN-γ/MEK/ERK-mediated activation of NF-κB (Bezzi et al., 2001; Mir et al., 2008; Barcia et al., 2011). This evidence concerns the gene NFKB1 and Parkinson disease.