MUL1, a ubiquitin ligase localized to the mitochondrial outer membrane, regulates multiple pathophysiological processes including apoptosis, mitophagy, mitochondrial dynamics, and innate immune responses.[39] Recent studies in rat models of ischemic stroke have shown that upregulation of MUL1 disrupts mitochondrial dynamics and exacerbates cerebral injury.[40] Similarly, Wang et al reported increased MUL1 protein levels during myocardial ischemia/reperfusion injury in rats. This evidence concerns the gene MUL1 and ischemic stroke.