Although it is tempting to speculate that autoantibodies or immune complexes might be responsible for such activation during SRC, we cannot formally rule out the effect of hypertension-induced hemodynamic shear-stress, which has also been shown to activate the classical pathway of the complement system on endothelial cells.[20] The increased FBb/FB ratio found in patient's serum suggested subsequent recruitment of the alternative pathway through the C3b feedback cycle, as previously described in lupus erythematosus.[21]. The gene discussed is SRC; the disease is hypertensive disorder.