The restoration of normal enucleation of red cells in Sox6-deficient mouse by postnatal day 10.5 may result from functional compensation of other Sox proteins (expressed at later developmental stages), since functional redundancy is a recurring theme with Sox proteins [13,45,46]. Moreover, erythropoiesis has already shifted from fetal liver to bone marrow by postnatal day 10.5. The accompanying change in the microenvironment of red cell production may permit normal enucleation. Identification of Sox6 downstream target genes and its interacting proteins will shed light on the role of Sox6 in red cell terminal differentiation and the enucleation process.