Since B32B3 treatment also almost completely abolished the ability of dCas9-VprBP wild type to repotentiate the growth activity of sgRNA 1 and 2-transfected G361 cells (Fig. 5d, e), these results strongly suggest that VprBP can function to stimulate the growth of melanoma cells in a kinase activity-dependent manner. The gene discussed is DCAF1; the disease is melanoma.