Previous reports had demonstrated that VEGF interacted with its receptors on the cellular membrane and phosphorylated AKT, subsequently activated mTOR, then up-regulated VEGF expression, and finally improved angiogenesis against cerebral ischemia [38, 39]; recent reports indicated that BDNF could bind with Tropomyosin receptor kinase B receptor and then activate AKT/mTOR signaling pathway which will result in neuroprotective effects, and was beneficial to maintain the endogenous neuronal progenitor pool and regulate new neuron development after stroke [23, 40–43]. This evidence concerns the gene AKT1 and stroke disorder.