The HOXA factor with transactivation potential in our experiments was HOXA5, which is expressed at high levels in the presence of MLL translocations12, 35 and has recently been shown to be critical for the leukaemic phenotype in a mouse model of CALM-AF10 driven T-ALL.23 Our data are consistent with a direct path from elevated HOXA levels to ectopic expression of LMO2, and therefore provide potential mechanistic insights into the dysregulation of transcriptional programmes in a larger fraction of T-ALL patients. The gene discussed is HOXA5; the disease is acute lymphoblastic leukemia.