In additional experiments, B32B3 treatment significantly impaired the suppressive activity of dCas9-VprBP wild type at INPP5J, ZNF750, and TUSC1 genes and dCas9-VprBP K194R kinase-dead mutant failed to exert any effects on transcription (Fig. 5b), clearly indicating the requirement of VprBP kinase activity for target gene silencing in melanoma cells. The gene discussed is DCAF1; the disease is melanoma.