Abundant evidence indicates that BET bromodomain, a family consists of BRD2, BRD3, BRD4, and BRDT, plays vital roles in the pathogenesis of specific leukemia as well as solid tumors, such as cervical cancer and bladder cancer.4, 5, 6 These proteins have been identified in several cellular programs contributing to neoplasia, including producing oncogenic fusion proteins and regulating the expression of tumor‐associated proteins, such as c‐Myc.7 Therefore, targeting BET proteins has emerged as a promising cancer therapeutic strategy. The gene discussed is DNER; the disease is neoplasm.