Since TNF‐α and NFκB are key mediators of NLRP3 priming, and pro‐IL‐1β acts as a substrate for NLRP3 inflammasome processing, this implies that PD pathology ‐ activates microglial cells and NLRP3 priming, which could be potentially mitigated by exercise intervention. This evidence concerns the gene NLRP3 and Parkinson disease.