Concomitantly, inflammatory cell infiltrates composed of macrophages, dendritic cells, and T and B lymphocytes have been found in PAH, implicating the participation of cytokines, including interleukin (IL)-1 and IL-6, and chemokines such as C-X3-C motif chemokine ligand 1 (CX3CL1) in a dysregulated proliferation of pulmonary artery smooth muscle cell (PASMC) and endothelial cell (EC) release of cytokines; the net effect is an increase in pulmonary vascular resistance [15]. This evidence concerns the gene CX3CL1 and pulmonary arterial hypertension.