The importanceof therapeutic targeting of AT sites has taken on increased significancewith the discovery that minor groove-binding heterocyclic diamidinescould inhibit the PU.1 transcription factor by binding upstream AT-richregions that are nearly ubiquitous in its promoter sites.6,24 With our small-molecule inhibitors, we found that PU.1 inhibitionis effective at disrupting AML cell growth in human cell lines andprimary AML patients’ cells in vitro and in vivo and is a newstrategy for the treatment of AML.6 The gene discussed is SPI1; the disease is acute myeloid leukemia.