EED and cancer: SAHA is widely accepted as an HDAC inhibitor, but its function as an EZH2 inhibitor has also been reported.5, 6 Recent studies have shown that EZH2 interacts with HDACs via EED (embryonic ectoderm development: as one of the polycomb repressive complex 2 component proteins) and that EZH2-mediated gene silencing is dependent on HDAC activity.20 In addition, another HDAC inhibitor, trichostatin A, completely abrogates the effects of EZH2 overexpression in cancer cells, thus supporting the function of SAHA as an EZH2 inhibitor.21