Furthermore, increased levels of GFAP would seem to be essential for a multitude of responses during Müller cell gliosis, such as the formation of glial scars, neurite growth, infiltration of monocytes, neovascularization, and the integration of cells in retinal transplants, as all these characteristics were found to be attenuated in GFAP- and vimentin-deficient mice, which are an experimental animal model of retinal detachment (Lewis and Fisher, 2003; Nakazawa et al., 2007; Bringmann et al., 2009). The gene discussed is VIM; the disease is retinal detachment.