That non-cytotoxic DNMT1 depletion produces large increases in total hemoglobin could thus mean that this approach is less suited to SCD subtypes with relatively high hematocrits at baseline, e.g., S-β+-thalassemia or S-C disease, even if RBC quality is improved concurrently by HbF induction. This evidence concerns the gene DNMT1 and Schnyder corneal dystrophy.