Regarding acute lung injury secondary to sepsis, an increase in ROS and RNS has been described, derived from the increase in the decoupling of eNOS and iNOS overexpression [123], which is associated with an increase and release of proinflammatory mediators such as TNF-α, IL-6 and IL-9 by bronchial epithelial cells. The gene discussed is IL6; the disease is Sepsis.