After generating sATF6-MER;Emx1-Cre (sATF6-KINeuron) mice with neuron-specific expression of sATF6 in the brain, we subjected these mice to transient filament middle cerebral artery occlusion (tMCAO), a stroke model, and found that forced activation of the ATF6 branch in neurons significantly reduced infarct volumes and improved neurologic function [18]. This evidence concerns the gene ATF6 and stroke disorder.