LYL1 and acute myeloid leukemia: Supporting this hypothesis, both the RASSF2 promoter CpG island34 and a downstream alternative transcription start site demonstrated chromatin co-occupancy of RUNX1-ETO, repressive histone deacetylases (HDAC1/2), and RUNX1-ETO transcription factor complex component LYL1 (ref. 7), in t(8;21) AML cells (Fig. 1d).