Furthermore, using a rat model, these investigators reported that the HERV-K dUTPase activated B cells, elevated pro-inflammatory cytokines IL-6, interleukin 1β (IL-1β), and tumor necrosis factor-α (TNF-α) in monocytes and pulmonary arterial endothelial cells (PAECs), increased pulmonary artery vulnerability to apoptosis, and induced PAH, suggesting that the HERV-K dUTPase contributed to sustained inflammation, immune dysregulation, and progressive obliterative vascular remodeling that occurs in PAH. This evidence concerns the gene IL6 and pulmonary arterial hypertension.