KLK6 and ischemic stroke: The reason for this phenomenon might ascribe to in situ reactive astrogliosis, which are proliferated astrocytes activated by transforming growth factor-α, ciliary neurotrophic factor, interleukin-1, interleukin-6, and Kallikrein-related peptidase 6 in penumbra following ischemic stroke [45], while the number of neuroblast (DCX+ cells) and mature neurons was dramatically increased in penumbra after ischemic stroke, demonstrating that targeting ASIC1a was a feasible strategy to promote NPC migration and differentiation into neuron.