,24 Moreover, silencing Sema3A gene expression in a murine model of OIR maintains neuroretinal function,24 suggesting that Sema3A may play a deleterious pathological role during retinal ischemia and in human DMI by contributing to capillary damage and subsequent neuronal malnutrition, build-up of waste products, and injury, resulting in progressive vision loss.9 Here, SEMA3A is linked to retinal ischemia.