There is a growing body of evidence to show that p38 MAPK is activated in neurons, astrocytes, and microglia after various types of ischemia [13-15], and its prolonged activation is associated with neuronal apoptosis and the production of pro-inflammatory cytokines, such as tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β), which are favored by acting as perpetrators in the central nervous system injury as well as conversely activating the p38 MAPK pathway [16,17]. This evidence concerns the gene TNF and ischemia.