As the final effect of opposed forces which repressed the cell cycle progression in G0/G1 phase in the IUGR fetal thymus by down-regulating expressions of both CDKs and cyclins, weakened GH/IGF signaling system in the IUGR fetal thymus was critical for abnormal IUGR fetal thymic cell growth and thymopoiesis, and was responsible for the retardation of the TECs growth and maturation of thymocytes. The gene discussed is IGF1; the disease is fetal growth restriction.