IL-1β may in part be released from infiltrating neutrophils and T cells in diseased pulmonary vessels, as evidenced by positive staining for key components of the inflammasome system, namely Nod-like receptor family pyrin domain containing 3 (NLRP3) and apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC) within these cells in chronic hypoxia-induced PAH mice [7]. This evidence concerns the gene IL1B and pulmonary arterial hypertension.