Another study showed that while cytokine profiles did not differ significantly between SSc patients at high and low risk for PAH, there was evidence of increased levels of VEGF-D in PAH groups patients compared to low-risk PAH groups and HC groups, and cytokines differentiating high-risk PAH patients from low-risk PAH patients were cytokines involved in modulating fibrosis and endothelial cell function including PAI-1, sICAM-1, and BDNF [53]. This evidence concerns the gene VEGFD and pulmonary arterial hypertension.