The heat shock protein 90 (HSP90) inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG) has demonstrated pre-clinical efficacy in AML, exhibiting cytotoxic effects in AML cell lines harboring FLT3 or BCR-ABL mutations and inducing apoptosis in primary AML cells.60, 61, 62 In a phase I study (NCT00103272)63 of 17-AAG plus bortezomib in 11 patients with relapsed/refractory AML, the MTDs were 150 mg/m2 and 0.7 mg/m2, respectively. The gene discussed is FLT3; the disease is acute myeloid leukemia.