Lalancette et al. demonstrated that targeted deletion of galectin-3 exacerbated ischemic damage and neuronal apoptosis after cerebral ischemia through the reduction of interaction between galectin-3 and insulin-like growth factor (IGF)-1, leading to downregulation of IGF-1 and suppression of resident microglia activation and proliferation in response to ischemic injury [47]. This evidence concerns the gene IGF1 and brain ischemia.