In contrast to the study of Li et al. [31], however, we found almost normally developed lungs at birth. Ptdsr -/-lungs showed, in comparison to wild-type, only a slight delay in maturation and were fully ventilated in neonates in most cases (Figure 3e,k). This demonstrates that Ptdsr-deficient mice can overcome the delay in embryonic lung differentiation and display normal lung morphology at birth. Thus, it would appear highly unlikely that Ptdsr -/- mice die from respiratory failure. Consistent with the observations of Kunisaki and colleagues [32], we found severely blocked erythropoietic differentiation at an early erythroblast stage in the liver (Figure 3f,3l), suggesting an explanation for the grossly anemic appearance that we observed in our Ptdsr -/- mice.