The initial specificity of BET BRDis allowed targeting of the ability of BET proteins to bind to acetyled lysine marks on histones found at active areas of the host genome, thereby inhibiting the cellular transcriptional dysregulation occurring in malignancies such as sarcoma and leukemia (Filippakopoulos et al., 2010; Dawson et al., 2011). This evidence concerns the gene DNER and sarcoma.