Collectively, our data support the hypothesis that the NLRP3 inflammasome is activated in early PD and AD, and lend further support to the idea that specific targeting of inflammasomes and/or their downstream constituents such as ASC, caspase 1 or cleaved gasdermin D37 warrants testing as a disease-modifying strategy for PD/AD38. The gene discussed is NLRP3; the disease is Alzheimer disease.