Finally, genetic evidence for Merlin’s function as a CRL4VprBP inhibitor comes from the author’s characterization of a panel of tumor-derived mutations, which fell into three catagories: those that impair Merlin’s ability to translocate into the nucleus, those that fail to bind VprBP, and those that bind VprBP, but do not inhibit CRL4VprBP activity. The gene discussed is DCAF1; the disease is neoplasm.