Thus, in addition to the classical approach aimed at suppressing detrimental M1 functions (i.e., production of TNF-α, IL-1β, monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-1α, and IL-6), preservation of the alternatively activated M2 phenotype may represent an innovative strategy for stroke neuroprotection, as demonstrated in mice lacking the class-A scavenger receptor (Xu et al., 2012) or the myeloid-specific mineralcorticoid receptor (Frieler et al., 2011). This evidence concerns the gene TNF and stroke disorder.