Corroborating these findings, work using genetics and small molecule BET inhibitors provide evidence for the involvement of Brd2 and/or other BET proteins in hematopoiesis [13,29,30], erythroid specification and transcriptome activation [13], hematological malignancies [17,18,30,34], and the modulation of pathways relevant to chronic kidney disease [19]. This evidence concerns the gene DNER and chronic kidney disease.