Recent studies showed that the NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome, an essential downstream target of HIF-1α after stroke, was extremely upregulated in the damaged thalamus of the CPSP model, and the NLRP3 inflammasome inhibitor was able to attenuate CPSP syndrome [16–19]. This evidence concerns the gene NLRP3 and stroke disorder.