Stroke-induced reactive gliosis protects the ischemic penumbra as shown by larger infarcts in mice in which reactive gliosis was attenuated by genetic ablation of GFAP and vimentin (GFAP−/−Vim−/−) [28, 32] and GFAP−/−Vim−/− astrocytes exhibit less efficient endothelin-3-induced blockage of gap junctional communication [28], lower levels of glutamine [64], lower glutamate transport [28] or increased vulnerability to oxidative stress [65]. Here, VIM is linked to stroke disorder.