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. Here, TUSC1 is linked to melanoma.