While this offers obvious therapeutic benefits, such as ROS-mediated DNA damage of tumor cells [29], in normal lung tissues, ROS can activate NF-κB signal transduction, leading to the expression of a variety of inflammatory genes for cytokines, IL-4, IL-5, IL-9, IL-15, and TNF-α, with the potential for significant lung parenchymal damage [30]. This evidence concerns the gene IL4 and neoplasm.