Some of the cellular and molecular events involved in the normal and precocious appearance of sucrase in jejunum of infant rats have been studied. Actinomycin D has been shown to inhibit (by 79%) the rise in sucrase activity usually seen after administration of hydrocortisone to 9-day-old rats. The precocious appearance of sucrase has also been studied with respect to the cytological localization of enzyme activity in the intestinal mucosa. Tissue was sectioned in a cryostat (transverse to the villi) and sucrase was assayed in homogenates prepared from the sections. By 24 h after administration of hydrocortisone to 9-day-old animals, sucrase was detectable only at the bases of the villi. During the subsequent 72 h the enzyme activity increased and spread along the villi at a rate consistent with that of cell migration. These data have lead to the conclusion that the action of glucocorticoids on enterocytes can occur only when the cells are in their proliferative phase. An ontogenic study of the ability of hydrocortisone to elicit jejunal sucrase showed that the tissue becomes increasingly responsive to the hormone with increasing age through the first and second postnatal weeks. Various hypotheses to explain this increase have been examined.