In vitro analysis showed that BSDL enhances the activation of human platelets — cells found in the blood that when activated are key to the formation of blood clots. In addition, in normal mice BSDL accumulated at sites of blood clot formation and in BSDL-deficient mice tail injury resulted in increased bleeding time. Further analysis revealed that BSDL mediated its effects on platelets in vitro and in vivo by binding a protein on the surface of platelets known as CXCR4. Indeed, inhibition of CXCR4 prevented BSDL-mediated human platelet activation, and eliminated BSDL accumulation and reduced blot clot size in mice. These data led the authors to conclude that the interaction between BSDL and CXCR4 might be a new target for therapies to treat conditions in which blood clots form inappropriately inside blood vessels, such as occurs in individuals with pancreatic cancer.-Journal of Clinical Investigation