At BCL11A we used PE2 to disrupt the GATA1 binding motif within the BCL11A erythroid enhancer that results in the induction of fetal γ-globin in erythroid progenitors and can ameliorate β-globinopathies like sickle cell disease and β-thalassemia (27,31). The gene discussed is BCL11A; the disease is sickle cell disease.