However, (i) we identified neither EHMT1 or EHMT2 in our LSD1 or HMG20B pulldown experiments, (ii) the enzymatic activity of LSD1 is not required for transcription repression at sites of GFI1 binding [8], and (iii) expression of a GFI1 zinc finger-HDAC1 fusion protein only partially rescued GFI1-mediated transcription repression following treatment of AML cells with an LSD1 inhibitor [8]. The gene discussed is EHMT2; the disease is acute myeloid leukemia.