In pre-clinical studies, potential neuroprotective and neuroplastic effects of SSRI on post-stroke recovery were largely attributed to modification of pathogenic mechanisms following ischemic stroke, such as ischemia-associated hyperexcitation, inflammatory processes in the post-acute phase, augmentation of cerebral blood flow, as well as enhancement of BDNF-expression and stimulation of adult neurogenesis in the subependymal zone and in the hippocampal dentate gyrus (4–10, 12–14). The gene discussed is BDNF; the disease is ischemic stroke.