By analogy with previous work showing that PKCε overexpression and activation by PMA mediates TACE induced-EGFR ligand release and promotes development of skin tumor in mice [22] and also based on the fact that enhanced PKCε activation and expression are required for non small cell lung cancer survival [43], [44], it is conceivable that the stimulation of PKCε by ROS in the smoke-exposed lung may be a major factor in the step of predisposing smokers to develop lung cancer. The gene discussed is EGFR; the disease is lung cancer.