DCAF1 and melanoma: Perhaps more important is the observation that there is a strong correlation between the level of dCas9-VprBP-mediated H2AT120p and the level of dCas9-VprBP-induced transcriptional inactivation and that dCas9-VprBP kinase dead mutant is unable to switch growth-regulatory genes from an active to an inactive transcriptional state in melanoma cells.