To further determine whether this de novo H3K27ac peak within the PVT1 locus is essential for maintaining MYC expression in BETi-resistant leukemia cells, we resorted to the CRISPR interference (CRISPRi) technique by fusing a catalytically-inactive Cas9 (dCas9) with a transcriptional repressor KRAB (the Krüppel-associated box; dCas9-KRAB)39. The gene discussed is MYC; the disease is leukemia.