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Myelodysplastic syndrome is a heterogeneous immunologic and epigenetic group of myeloid disorders with variable propensity for acute myelogenous leukemia (AML) conversion. Treatment is limited to growth factors, lenalidomide for 5q deletion MDS, and best supportive care for low-risk disease. Allogeneic transplantation and epigenetic therapy are conventionally considered alternatives for high-risk MDS. Inflammation, epigenetic, and cytogenetic participate in disease initiation. However, how these factors interface to develop vulnerability for the disease is largely unknown. In this review, we describe current inflammatory, immunologic, and molecular features that integrate mechanistic potential effectors for MDS.

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