Decitabine is a deoxycytidine analog that rapidly enters into cells by a nucleoside-specific transport mechanism. It is then phosphorylated by deoxycytidine kinase and converted to the active triphosphate form, 5AZA-dCTP, a substrate for DNA polymerase alpha. 5AZA-dCTP is incorporated into DNA and inhibits DNA methylation as inactivating DNA methyltransferase. Decitabine is s-phase specific. A recent study randomized 170 patients with MDS to receive either decitabine or best supportive care. Patients who were treated with decitabine achieved a significantly higher overall response rate (17%) including complete responses (9%), compared with supportive care (0%). Responses were durable and were associated with transfusion independence. Patients treated with decitabine had a trend toward a longer median time to acute myelogenous leukemia (AML) progression or death compared with patients who received supportive care alone. Responses in AML have also been demonstrated with 14% complete responses and 8% partial responses in one study . Decitabine has been used in combination with cyclophosphamide and busulfan as preparative regimen in patients with AML. This regimen was associated with a high response rate, with 40% of patients with AML being still in remission more than three years after transplantation. The total dose of decitabine ranged from 400 mg/m2 to 800 mg/m2. No decitabine dose-limiting toxicity was documented. The combination of fludarabine and busulfan has been well established as a transplant regimen and is associated with a reduced regimen-related toxicity. The combination of fludarabine and busulfan is the current standard of care for AML patients undergoing allogeneic transplantation at HUMC. In this study the investigators will be using the combination of reduced-intensity fludarabine and busulfan along with decitabine 300 mg/m2.