Recently, special attention has attached to the role of tumor necrosis factor receptor-associated factor 6 (TRAF6) in the response of the CNS to traumatic injuries [30], with the detection of significant increase in TRAF6 levels in traumatic brain injury and ischemic stroke models, which markedly inhibited autophagy and accelerated disease progression [[31], [32], [33], [34]]. This evidence concerns the gene TRAF6 and ischemic stroke.