To assess the relevance of high mannose N-glycan display for RBC uptake in vivo, we exploited the heterogeneity of sickle cell disease arising from the interactions of HbS with other mutations in the globin loci (such as HbC, α-thalassemias, and β-thalassemias) that also protect against malaria.13 If mannoses were phagocytic ligands in sickle cell disease, higher levels of mannose exposure should correlate with more severe anemia. The gene discussed is KRT88P; the disease is anemia.