The apoptosis repressor with caspase recruitment domain (ARC) plays a critical role in extrinsic apoptosis initiation via death receptor ligands, physiological stress, infection response in a tissue-dependent manner, endoplasmic reticulum (ER) stress, genotoxic drugs, ionizing radiation, oxidative stress, and hypoxia. Recent studies have suggested that regulating apoptosis-related pathways can improve outcomes for patients with neurological diseases, such as hemorrhagic stroke. ARC expression is significantly correlated with acute cerebral hemorrhage. However, the mechanism by which it mediates the anti-apoptosis pathway remains poorly known. Here, we discuss the function of ARC in hemorrhagic stroke and argue that it could serve as an effective target for the treatment of hemorrhagic stroke.