Correlational evidence and nonselective manipulations aiming at inhibition of Cx43 function in astrocytes led to the idea that Cx43 contributed to the amplification of ischemic damage, as the treatment with octanol, a nonselective connexin and gap junction blocker, reduced the infarct size in rat models of cerebral ischemia by carotid or middle cerebral artery occlusion (Rawanduzy et al., 1997; Rami et al., 2001). Here, GJA1 is linked to brain ischemia.