Although αSYN aggregates are considered primary and master disease-associated inflammatory triggers in PD, compelling experimental evidence supports an independent pathogenic role of TNFα and the PGE2-producing enzyme cyclooxygenase 2 (COX2), suggesting that in addition to being part of a large panel of effector molecules derived from activated glial cells or injured neurons, these inflammatory cues are instrumental in neuronal cell death possibly through regulation of microglia-associated inflammation and toxicity [71–75]. The gene discussed is TNF; the disease is Parkinson disease.