DCAF1 and melanoma: 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 (Figure 5B), clearly indicating the requirement of VprBP kinase activity for target gene silencing in melanoma cells.