The switch from fetal (HBG) to adult (HBB) -globin gene transcription in erythroid cells serves as a paradigm for a complex, clinically relevant developmental gene regulatory program. We previously identified HIC2 as a regulator of the switch by inhibiting the transcription of BCL11A, a key repressor of HBG production. HIC2 is highly expressed in fetal cells but the mechanism of its regulation is unclear. Here we report that HIC2 developmental expression is controlled by miRNAs, as loss …