Indeed, this cancer-associated mutated UVRAG, which lacks CEP63-binding ability, is more than just a relic of UVRAG inactivation, it instead disturbs the association of endogenous UVRAGWT with CEP63, presumably by displacing endogenous active UVRAG from the centrosome and/or by titrating out an unknown regulator into nonfunctional complexes. Here, CEP63 is linked to cancer.