Two physiological maturations of the rat liver are presented in this paper. The ability for glycogen storage depends in vivo on the presence of endogenous circulating glucocorticoids. Similarly, in vitro, primary cultures of fetal hepatocytes store glycogen only in cortisol-supplemented media. Cortisol exerts its effects by enhancing the activity of the synthetic pathway of glycogen metabolism. Glucocorticoids also control the erythropoietic tissue of the fetal liver. They reduce the self maintenance ability of the stem cell pools and accelerate the maturation processes. Under their stimulation the liver becomes the main erythrocyte producer in the fetus and progressively loses its erythropoietic tissue, probably by exhaustion. The synchronism in the maturations of the two major cellular populations is essentially due to the fact that their common inducers, the corticosteroids, are suddenly released in enhanced amounts on and after 17–18 days of gestation.