We and others previously demonstrated that mice carrying null mutations in genes encoding glial fibrillary acidic protein (GFAP) and vimentin (GFAP−/−Vim−/− mice) have astrocytes devoid of astrocyte intermediate filaments [7, 8] and exhibit better posttraumatic regeneration of neuronal synapses and axons [9, 10], improved functional recovery after spinal cord injury [11], reduced photoreceptor degeneration in the retinal detachment model [12], and reduced pathological neovascularization in oxygen-induced retinopathy [13]. Here, GFAP is linked to retinal detachment.