This view was supported by our present evidence including (i) the serum cortisol level in the human IUGR umbilical blood was increased; (ii) normal human WJ-MSCs treated with excessive cortisol displayed similar features as WJ-MSCs from IUGR individuals, when undergoing the chondrogenic differentiation in vitro; (iii) The WJ-MSCs from IUGR individuals presented a poor capacity for chondrogenic differentiation and subsequent increased susceptibility to an osteoarthritis-like phenotype, due to the decreased H3K9ac and expression levels of TGFβRI induced by excessive cortisol though GR/HDAC4. The gene discussed is NR3C1; the disease is fetal growth restriction.