Myelodysplastic syndromes (MDS), clonal hematopoietic stem-cell disorders mainly affecting older adult
patients, show ineffective hematopoiesis in one or more of the lineages of the bone marrow. A number of
MDS progresses to acute myeloid leukemia (AML) with the involvement of genetic and epigenetic
mechanisms affecting PI-PLC \u3b21. The molecular mechanisms underlying the MDS evolution to AML are
still unclear, even though it is now clear that the nuclear signaling elicited by PI-PLC \u3b21, Cyclin D3, and Akt
plays an important role in the control of the balance between cell cycle progression and apoptosis in both
normal and pathologic conditions. Moreover, a correlation between other PI-PLCs, such as PI-PLC \u3b23, kinases
and phosphatases has been postulated in MDS pathogenesis. Here, we review the findings hinting at the role
of nuclear lipid signaling pathways in MDS, which could become promising therapeutic targets
