SLC9A1 and Stroke: Considering that the detrimental ROS and nitric oxide (NO) from reactive astrocytes can in turn to promote the activation of microglia [57, 58], the effects of pharmacological blockade of NHE1 protein in attenuating microglial activation could be indirect through reducing reactive astrogliosis and/or via directly inhibiting microglial NHE1 activity, the latter was shown to be involved in stroke-mediated proinflammatory microglial polarization [17].