Recent studies demonstrate that the JAK1/2 inhibitor, Ruxolitinib, reduces the release of proinflammatory factors by inhibiting the activation of the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome in macrophages, as well as the JAK2/STAT3 pathway, thereby ameliorating brain edema after stroke (Table 4) (178). The gene discussed is STAT3; the disease is stroke disorder.