GJA1 and retinal ischemia: Research indicates that increased formation of gap junctions by Cx43 in models of retinal ischemia/reperfusion injury can facilitate the spread of inflammatory molecules between cells, thereby exacerbating damage to RGCs.[14] Furthermore, substantial ATP released by astrocytes via Cx43 can stimulate microglia to adopt a pro‐inflammatory M1‐like phenotype, which accelerates neuroinflammation and RGC apoptosis.