A recent study by Rust et al. used a stroke model in mice with Nogo-A or its receptor S1PR2 gene deletion and found that it could improve the regeneration and repair of blood vessels after cerebral ischemia in mice and reduce neurological deficits, suggesting that the anti-Nogo-A treatment can improve the repair of blood vessels and nerves after ischemic central nerve injury [22]. Here, S1PR2 is linked to stroke disorder.