A relationship between reactive oxygen production and IL-4 function was postulated by Sharma and colleagues [41] who suggested that exposure of the A549 human lung adenocarcinoma cell line to IL-4 activated NOX1 to generate ROS within minutes, without changing NOX1 expression levels; they suggested that subsequent, ROS-related inhibition of protein tyrosine phosphatase activity could play an important, enhancing role in IL-4 signaling. The gene discussed is IL4; the disease is lung adenocarcinoma.