Abstract
The anaemia of MDS is multifactorial with intramedullary ineffective erythropoiesis resulting from an imbalance between erythroid proliferation, differentiation and apoptosis in favour of initial hypercellularity with high cell death through to a lower cellularity, lower death state with the eventual evolution of the leukaemic clone in many patients. The fundamental molecular abnormality(ies) in MDS, which produce the milieu for the heterogeneous molecular insults (described (e.g., oncogene mutations) remains elusive. Many questions such as why MDS red cells are macrocytic and what are the precise cellular and molecular mechanisms of ineffective erythropoiesis remain unanswered but future study of the erythroid lineage should provide molecular clues to the earliest abnormalities in the pathogenesis of MDS.