In the same experiment, phenocopying the effect of reader bromodomain inhibitors, combinatorial treatment with CBPD-409 and thalidomide still triggered the loss of bromodomain-dependent H3K27ac and repressed MYC expression (Figures 5E–F), suggesting the residual H2BNT acetyltransferase activity of bromodomain-inhibited p300/CBP continues to support the expression of important cancer-promoting genes. This evidence concerns the gene MYC and cancer.