Furthermore, genetic ablation of AKAP1 was found to exacerbate stroke‐related injury in mice.100 The deletion of Akap1 in mice reduced phosphorylation of Drp‐1 on Ser637, which impaired fission.100 Reduced Drp1 phosphorylation in Akap1‐/‐ mice contributed to Ca2+ dysregulation, dysregulation of complex II, and increased ROS production in response to excitotoxic stress.100 This suggests that the PKA/AKAP1 mitochondrial signaling nexus is crucial to regulating stress responses and preserving optimal organelle function in the brain. This evidence concerns the gene AKAP1 and Stroke.