Although in earlier studies with preclinical AML models, a small molecule SGI-1776 PIM/FLT3 inhibitor exhibited promising activity, the compound failed clinical testing due to a narrow therapeutic window and cardiac toxicity (related to off-target effects of the inhibitor and its metabolites - inhibition of the potassium channel hERG) [25, 35]. Here, FLT3 is linked to acute myeloid leukemia.