Neutrophil extracellular traps (NETs), comprised of the decondensed extracellular chromatin network of activated neutrophils, and necessary for catching and killing of microbes in innate immunity, were found to positively affect angiogenesis in a preclinical model of pulmonary hypertension through the upregulation of intercellular adhesion molecule 1 (ICAM-1) expression, affecting VEGF-signaling and endothelial cell migration [48]. This evidence concerns the gene ICAM1 and pulmonary arterial hypertension.