Deletion of the erythroid specific enhancer of BCL11A (Bauer et al., 2013), a transcriptional repressor that inhibits fetal hemoglobin (Hb-F) expression, can enhance the levels of Hb-F, resulting in phenotype alleviation of sickle cell disease (SCD) and β-thalassemia. This evidence concerns the gene GSTM1 and sickle cell disease.