Contributing events, such as inflammation at the stroke site, allowing E-selectin to be expressed by the inflamed endothelium, S1P2 to reduce the extent of tight junctions established by S1P1, and L-selectin expression on activated lymphocytes may all contribute towards TH and TREG cell rolling and diapedesis through vessels traversing cerebral areas possessing S1PHIGH concentrations. Here, S1PR2 is linked to stroke disorder.