In conclusion, pharmacogenomics of HbF induction in response to thalidomide should be considered in further studies on β-thalassemia and SCD patients in order to confirm the contribution of the identified SNPs in HBG2 and HBS1L-MYB in the response to thalidomide and the hypothesis of a lack of correlation between response to thalidomide and the HBG2 XmnI polymorphism. This evidence concerns the gene HBG2 and Schnyder corneal dystrophy.