Taken together, these data indicated that endogenous PTH deficiency could inhibit chondrocyte proliferation and differentiation at the callus whereas exogenous PTH could phosphorylate CREB, promote chondrocyte proliferation and attenuate impaired fracture healing resulting from endogenous PTH deficiency. The gene discussed is CREB1; the disease is hyperinsulinemic hypoglycemia, familial, 4.