Ding P, et al. - Researchers sought for the pathogenesis of glucocorticoid (GC)-induced avascular necrosis of the femoral head (ANFH) via determining the effects of GCs on EPCs given their important role in the progression of GC-induced ANFH. The peripheral blood of ANFH patients and healthy controls were assessed for circulating EPCs by Ficoll-density gradient centrifugation. Patients with GC-induced ANFH displayed significantly decreased number and functions of EPCs. For the first time, in vitro study revealed that except extremely high concentrations, low to medium concentrations of GCs have no significant effects on EPCs’ growth. However, significant impairement of EPC angiogenic function in vitro was observed in correlation to GCs, even at low concentrations. This study also suggests that GCs suppress EPCs’ angiogenesis possibly via a novel mechanism including downregulation of CXC chemokine receptor 7 and its downstream Akt/GSK-3β/Fyn pathway in EPCs.