Phosphorylation of eNOS at ser 1177 in the aorta from lpr_Control (0.45 ± 0.09 a.u.)relative to the total eNOS was approximately 50% lower than the aortas from MpJ_Control (1.00 ± 0.16 a.u.)(Figure 2A,D), suggesting the potential mechanism of endothelial dysfunction in SLE. The gene discussed is NOS3; the disease is endothelial dysfunction.