Vascular smooth muscle cell (VSMC) phenotypic remodelling is pivotal to neointimal hyperplasia (NH), a common pathological response to vascular injury. COPS5/CSN5/JAB1 harbours the deneddylase of the COP9 signalosome (CSN) holocomplex but also has deneddylation-independent function. The role of COPS5 in VSMCs remains obscure.