However, more compelling evidence supporting the involvement of neuroinflammation in PD pathogenesis relies on genome-wide association studies, which have found a genetic association with PD susceptibility in the human leukocyte antigen region (Nalls et al., 2014) and other polymorphisms related to the immune system including TNF, TNFR1, IL-1β, triggering receptor expressed on myeloid cells 2, IL-1 receptor antagonist and CD14 (Hirsch and Hunot, 2009; Rayaprolu et al., 2013). The gene discussed is CD14; the disease is Parkinson disease.