In the acute phase of cerebral I/R injury, SP600125 treatment reduced cerebral infarction by inhibiting the expression of inflammatory mediators including TNF-α, IL-1β, IL-6, and matrix metalloproteinase-9 and downregulating the mitochondria-mediated apoptotic pathway in the ischemic area [53–55]. The gene discussed is TNF; the disease is cerebral infarction.