To this end, we provide evidence from primary human and mouse microglia exposed to canonical and non-canonical stimuli and/or α-syn fibrils as well as from aged human C-terminally truncated (1–120) α-syn transgenic (SYN120 tg) mice, which exhibit α-syn aggregation and DA deficiency [37, 38], to suggest that DA receptor binding can indeed block PD-relevant NLRP3 inflammasome activation. The gene discussed is NLRP3; the disease is Parkinson disease.