 These include transient spikes in monocyte- and macrophage-associated inflammatory mediators and temporary increases in the proteins vascular endothelial growth factors (VEGF) and angiopoietin-2.The impairment of endothelial cells in laboratory conditions provoked by serum taken from patients who were having episodes of SCLS is also suggestive of biochemical factors at work.There is no evidence that SCLS is hereditary, and the role of specific gene defects in patients with SCLS, which might program their endothelial cells for an overreaction to external stimuli, has not been established.