While further studies are required, to demonstrate a direct contribution of NLRP3/TXNIP interaction to PD-like pathology, these studies raise the possibility that TXNIP and the NLRP3 inflammasome may be subject to regulation by both mitoROS and ERS and that the TXNIP/NLRP3 signaling axis may represent a feed-forward loop contributing to the enhancement of the αSynagg-induced neurotoxic microglial activation state. The gene discussed is NLRP3; the disease is Parkinson disease.