The ischemic stroke is considered one of the major causes of death and permanent disability in industrialized countries.  The brain ischemia is produced as a consequence of a transient or permanent decrease of the cerebral blood flow that alters the level of the neurotransmitter glutamate after stroke, leading to irreversible neuronal damage. In addition, inflammation exacerbates neuronal loss preventing recovery in the acute phase of the ischemic episode. Recently, the same team of researchers reported the role played by the exchanger cystine/glutamate (System xc-) in the alteration of the glutamate levels that triggers neuronal damage after stroke. The present research evidences the role of this system during brain inflammation following ischemic stroke, thereby identifying a novel target for the theranostics of neuroinflammation.