One possibility for this to occur is by use of a regimen that combines an optimal CDK2 inhibitor that limits the ability of supernumerary centrosomes to cluster as with a PLK4 antagonist, which we reported to over-duplicate centrosomes in cancer cells.39 Such studies are relevant to translational cancer research in that pre-clinical activity could provide a rationale for the design and conduct of a future CDK2 inhibitor trial. The gene discussed is PLK4; the disease is cancer.