In this study, we aimed to investigate the role of ERK1/2 after acute cerebral ischemia in transgenic mice using constitutive overexpression of proteins that impact on ERK activation, i.e., mice that ubiquitously overexpress ERK2wt, RKIPwt, or RKIPS153A under the control of the “CAG” promoter (cytomegalovirus enhancer, β-actin intron, and bovine globin poly-adenylation signal promoter) [19,20]. This evidence concerns the gene MAPK1 and brain ischemia.