In view of the ischemia, generation of inflammation, oxidative stress and reactive oxygen species (ROS) are the major contributors for progressive brain damage after AHS and, based on the aforementioned issues, it is praiseworthy to investigate whether DPP4 inhibitor therapy really limits the brain hemorrhagic volume and preserves neurological function, as well as improves prognostic outcome after AHS. The gene discussed is DPP4; the disease is mitochondrial DNA depletion syndrome 4a.