However, when neurons suffer from ischemic stroke, the protein level of OMA1 increases, leading to increased OPA1 cleavage at the S1 site mediated by it, and increased S1-OPA1 aggravates ischemia-induced neuronal mitochondrial fragmentation and dysfunction in a GTPase-dependent manner, eventually leading to ischemia-reperfusion injury of neurons (Fig. S7). This evidence concerns the gene OPA1 and ischemic stroke.