Very recently, our group created a protein-based PROTAC to deplete endogenous BCL11A, a transcription factor validated as a therapeutic target for the hemoglobin disorders sickle cell disease and β-thalassemia.40 Our design fused a nanobody binder specific for BCL11A to the cell-permeant miniature protein ZF5.3 (ref. 105 and 106) and to tSPOP, the catalytic domain of the E3 adapter protein SPOP. This evidence concerns the gene BCL11A and hemoglobinopathy.