These results are consistent with reports of decreased activation of the PI3K–Akt pathway and increased activation of the Mek–Erk pathway in peripheral nerves of Pmp22-overexpressing rat models of CMT [31] and the disrupted maturation of SCs because of an imbalance between the PI3K–Akt and Mek–Erk pathways that contributes to the pathogenesis of CMT1A [32]. This evidence concerns the gene MAPK1 and Charcot-Marie-Tooth disease type 1A.