Poor prognosis occurs in AML patients whose blasts exhibit repressed expressions of p16INK4A/CDKN2A and DAPK1, on a background of HOXA9/MEIS1 over-expression (HS Boswell, unpublished data).[4, 23] These features coincide with ID1 hyperexpression, which overlaps with these repressed genes, and repressed RUNX3.[30] Therefore, we performed focused gene expression analysis on available pretreatment blasts from patients on the first trial, as test cohort (Figure 1). Here, MEIS1 is linked to acute myeloid leukemia.