In our study, the significant increase of sphingomyelin and sphingosine caused abnormal sphingomyelin metabolism which up-regulated S1P expression, increased CD62P expression, intensified platelet activation, enhanced Bcl-2 level, inhibited cleaved Caspase-3 expression, induced cell necrosis and apoptosis - mechanisms which underlie the pathophysiology of stroke. The gene discussed is SELP; the disease is stroke disorder.