Given the fact that it has been demonstrated that a microenvironment dominated by pro-inflammatory cytokines favors polarization to M1 microglia and prevents an M2 switch [108] and that ablation of Npas4 resulted in increased IL-6 and TNF-α cytokine levels in the brain following ischemia [26], it is possible that microglia could be primed toward the M1 state in Npas4−/− mice which maybe the underlying cause of the increased stroke-induced brain injury and inflammation observed in these animals. This evidence concerns the gene TNF and stroke disorder.