Strikingly, naturally occurring HPFH mutations within the −115 region (−117, −114, and the 13 bp deletion) that span the BCL11A-binding site (TGACCA: from −118 to −113) impair BCL11A’s ability to directly bind to the promoter and thus elevate HbF levels8,25,26, prompting gene editing approaches to disrupt this motif for treating β hemoglobinopathies. The gene discussed is BCL11A; the disease is hemoglobinopathy.