Iron overload is a frequent consequence in transfusion-dependent myelodysplastic syndromes (MDSs), which often requires iron chelation therapy (ICT). Interestingly, ICT may sometimes induce a hematologic improvement that leads to significant reduction or complete interruption of blood transfusions. This phenomenon has been recently described in MDS treated with the new oral chelator deferasirox. Here we briefly review the literature about this phenomenon and discuss the possible biological mechanisms underlying hematologic effects of deferasirox in MDS, starting from a new paradigmatic case in whom both hemoglobin level and platelet count improved, inducing transfusion-independence, soon after starting the treatment with deferasirox.
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