Freitas-Andrade et al. have demonstrated that the pharmacological blockade of Cx43 hemichannels with TAT-Gap19 significantly decreased infarct volume in an animal stroke model, and the detrimental hemichannel activity following ischemic stroke was linked to MAPK phosphorylation of sites at the Cx43 C-terminus [76]. This evidence concerns the gene GJA1 and stroke disorder.