Since enhancer architecture is a critical component of cell identity, it is possible that, moving forward, an assessment of a tumor’s baseline enhancer activity could serve as a potential epigenomic biomarker of response to BET inhibition and aid in tailoring treatment in a patient-specific manner (Hnisz et al., 2013; Kron et al., 2014). The gene discussed is DNER; the disease is neoplasm.