HDAC5 and breast neoplasm: For example, MLL is required for proangiogenic endothelial cell functions through regulating the expression of Hox genes [35]; silencing of HDAC5 exhibits a proangiogenic effect through up-regulating the transcription of FGF2 and SLLT2 [36]; GATA1 recruits SET7 to enhance the expression of VEGF in breast cancer cells, which promotes breast tumor angiogenesis [37].