UCHL1 and lung cancer: Ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) protein deubiquitinates and upregulates NOX4 to generate H2O2 and the overexpression of UCH-L1 promoted the invasive potential of the B16F10 lung cancer cell line via regulating the upstream kinase Akt, suggesting that ROS are related to cancer aggressiveness in various pathways66.