Several cellular targets (direct or indirect) have been identified for UCH-L1 in different types of malignancies: UCH-L1 contributes to p27 (Kip1) degradation via its interaction and nuclear translocation with JAB1 (COPS5) in lung cancer cells [10]; the β-catenin oncogenic pathway is activated by UCH-L1 [11]; UCH-L1 manipulates the mTOR-mediated protein biosynthesis and is required for MYC-driven lymphomagenesis in mice [12]. Here, COPS5 is linked to lung cancer.