Hormonal imprinting occurs perinatally when the developing receptor and the appropriate hormone meet each other. The presence of related molecules in this critical period causes misimprinting. Ligands bound to a member of the steroid-thyroid receptor superfamily can disturb the normal maturation of other members of the family, which is manifested in altered binding capacity of the receptor and decreased or increased response of the receptor-bearing cell for life. Excess or absence of the hormone also can cause misimprinting. Treatments once a week for 3 weeks of nursing rat mothers with 6 mg/animal all-trans retinol/dose caused faulty imprinting manifested in significantly reduced density (Bmax) of thymic glucocorticoid receptor in male and female adult progenies alike. 0.03 mg all-trans retinoic acid treatment of nursing mothers was ineffective. Receptor affinity (K_d)wasun-changed in both cases as well, as the binding values of uterine estrogen receptors. The results of the experiment call attention to the transmission of imprinter molecules by breastmilk to the progenies, which can cause lifelong alterations at receptorial level and points to the human health aspect. Possible reasons for the differences between retinol and retinoic acid effects and in the sensitivity of receptors are discussed.