Dear Editor, Patients with myelodysplastic syndromes (MDS) and a medullary blast count of more than 10% have a median survival of about 1 year. Intensive treatment approaches like induction chemotherapy and allogeneic stem cell transplantation offer a curative approach, but are not feasible for the vast majority of patients due to age and/or comorbidities. During recent years several new agents are being tested, such as farnesyl transferase inhibitors (tipifarnib, lonafarnib), immunomodulatory drugs (lenalidomide, thalidomide), DNA methyltransferase inhibitors (5-azacitidine, decitabine), and histone deacetylase (HDAC) inhibitory drugs to ameliorate the poor prognosis of patients affected by this disease. We here report on a 70-year-old male, diagnosed as RAEB II in January 2002. Our patient received five of the above mentioned substances sequentially and responded to three of them. Now, 7 years later he is still alive and in good condition. The patient was diagnosed as RAEB II in January 2002 and was transferred to our department in June 2002. Bone marrow puncture revealed a blast count of 10–15% and a normal karyotype. At that time he was transfusion-independent, but showed rapidly deteriorating platelet counts. The IPSS risk category was intermediate-II. Clinically, he suffered from fatigue, night sweat, and loss of weight. Secondary diagnoses were coronary heart disease, arrhythmia with atrial fibrillation, and a history of malignant melanoma of the temple (1997). Before retiring, he worked at the chemical industry and had a history of benzene exposure; therefore, his bone marrow disease might be regarded as secondary MDS, which is often connected with an adverse course of disease, even though his karyotype was normal. At least, his pension insurance officially recognized the MDS as occupational disease. His father had suffered from esophageal cancer and his mother died of kidney cancer. In July 2002, we initiated a therapy with thalidomide starting with 100 mg per day up to 400 mg per day. The treatment was poorly tolerated and had to be cancelled only 1 month later due to fatigue and drowsiness. A follow-up examination in September 2002 showed a stable disease with a still increased marrow blast count of 13%. Platelet count at that time had decreased to a minimum of 21,000/μl and hence we included him in a multicenter phase II trial with the farnesyl transferase inhibitor (FTI) tipifarnib [1]. Cell counts at start of treatment were: platelets 28,000/μl, Hb 11.1 g/dl, and ANC 700/μl. He started on a dosage of 600 mg p.o. per day. Already after two treatment cycles, he achieved a partial remission with improvement of peripheral cell counts and complete bone-marrow (BM) blast clearance (blast count, 3%). Maximum ANC was 1,900/μl, Hb 13.5 g/dl, and maximum platelet count was 263,000/μl. Between October 2002 and December 2004, he received 29 cycles of tipifarnib until the therapy was stopped due to polyneuropathy. At time of discontinuation, bone marrow examination revealed progression into RAEB I (BM blast count, 7%). The disease status remained stable and our patient did not develop transfusion dependency for about 1 year without further treatment. In October 2005, a progression into RAEB II occurred with a blast count of 12% and progressive thrombocytopenia was observed and consequently the patient was included in a multicenter study on the demethyAnn Hematol (2009) 88:1141–1144 DOI 10.1007/s00277-009-0730-x