The effect of azacitidine is not immediate in all patients, and it is therefore necessary to proceed with a minimum 5-6 cycles to determine whether the patient has a response to treatment. At present, azacitidine is the standard of care for all patients with high-risk MDS and AML with <30% blasts, who cannot be offered curative treatment. Unfortunately, most patients who respond to treatment later relapse and die of their disease. The mechanism behind the clinical efficacy of azacitidine is not fully elucidated and may be multiparametric. The hypomethylation results in re-expression of tumor suppressor genes that may serve as a possible mechanism for growth arrest. In addition, an up-regulation of cancer testis antigens (CTA) has been observed during treatment, which could lead to increased immune recognition of tumor cells, and hence immune-mediated tumor cell killing.