The A1 phenotype is stimulated by proinflammatory mediators, such as tumor necrosis factor (TNF-α), interleukin beta (IL-β), and ROS production, and is abundantly present in most major neurodegenerative disorders, in contrast to the ischemia-induced phenotype (A2), which is upregulated by neurotrophic factors and primarily influences neuronal regeneration and reparation [29]. This evidence concerns the gene TNF and ischemia.