Neuroinflammation has proven to be responsible for the secondary brain injury after intracerebral hemorrhage (ICH), and its mechanisms are characterized by features of microglial activation and neutrophil infiltration to release proinflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, myeloperoxidase (MPO), and other toxic chemicals (1–3). This evidence concerns the gene TNF and intracerebral hemorrhage.