This hypothesis is supported by the increased expression of TLR2 observed in the brain and peripheral tissues of patients with PD [27,28,29] and the suppression of pathologic changes in inflammatory responses and α-synuclein aggregate accumulation in the brains of TLR2-knockout (TLR2-KO) in the SNCA transgenic mice [23]. The gene discussed is TLR2; the disease is Parkinson disease.