Growing histological and biomarker evidence demonstrates that early and persistent inflammation is a critical component of PAH, with several studies observing circulating autoantibodies, elevated levels of macrophage inflammatory protein-1α, and increased pro-inflammatory cytokines levels such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor (TNF)-α in experimental and clinical PAH [3,14]. This evidence concerns the gene IL1B and pulmonary arterial hypertension.