Additionally, TNF-α and IL-1β trigger an NF-kB-driven intracellular signaling cascade in lung-infiltrated Th17 lymphocytes, enhancing the production of IL-17, which promotes the production of ROS, elastases, and matrix metalloproteinases (MMPs) in neutrophils, exacerbating tissue destruction and remodeling in the lungs of COPD patients [31]. The gene discussed is IL1B; the disease is chronic obstructive pulmonary disease.