p38 MAPK is phosphorylated on both threonine 180 (Thr180) and tyrosine 182 (Tyr182) residues during oxidative stress [51], and according to our data, ischemic brains showed an apparent increase in the levels of activated p38 throughout the acute stroke phase in the core area after tMCAO, while PCE-treated mice had suppressed levels of activated p38 in both the core and penumbra areas. This evidence concerns the gene MAPK14 and Stroke.