Similarly, KCa3.1 blockers have been demonstrated to reduce microglia activation and cytokine production in MOG‐induced experimental autoimmune encephalomyelitis (EAE) (Reich et al., 2005), prevent microglia activation and retinal ganglion cell degeneration after optic nerve transection (Kaushal et al., 2007), and to reduce infarct area in models of traumatic brain injury (Mauler et al., 2004) or stroke (Chen et al., 2011). Here, MOG is linked to brain injury.