β-thalassemia and sickle cell anemia (SCA) are hemoglobin diseases caused by abnormal β-globin

occurring in South-east Asia

South Asia

North Africa and the Mediterranean region with different degrees. Elevated fetal hemoglobin (HbF) levels can significantly improve their clinical symptoms. B-cell lymphoma/leukemia 11A (BCL11A)

a zinc finger structure transcription factor

plays an important negative regulatory role in fetal-to-adult hemoglobin expression. Down-regulated BCL11A activates γ-globin

so as to increase fetal hemoglobin expression

alleviating clinical symptoms of β-thalassemia and SCA. This article focuses on the mechanism of BCL11A on γ-globin

and the treatment of β-thalassemia and SCA based on BCL11A

thereby providing a theoretical basis for the study of β-globin disease.