Thus, context-dependent consequences of CXCR4 activation with CXCL12 may explain that CXCL12 administration desensitized phenylephrine-mediated vasoconstriction of isolated arteries and reduced blood pressure in a model of isolated hemorrhagic shock in spontaneously breathing rats, whereas CXCL12 sensitized the phenylephrine induced blood pressure response in normal rats and stabilized hemodynamics in the present ARDS model34,37. The gene discussed is CXCR4; the disease is acute respiratory distress syndrome.