The impact of ERK1/2 signaling in stroke was analyzed using different MEK/ERK1/2 inhibitors [9,10] or by transient overexpression of the endogenous Raf-kinase inhibitor protein (RKIP) [11,12], or agents that stimulate the Raf/MEK/ERK1/2-cascade such as β-hydroxybutyrate [13] or microribonucleic acid-1 (miR-1) [14]. This evidence concerns the gene PEBP1 and stroke disorder.