After cerebral ischemia, they can be rapidly activated and polarized towards two main phenotypes [6], the former being classically activated M1 microglia/macrophages, which secrete pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin 1 beta (IL-1β), and then mediate the inflammatory cascade reaction, aggravating tissue damage. The gene discussed is TNF; the disease is brain ischemia.