Major conclusions from these studies are that receptor occupancy usually directly governs biologic responses to corticosteroids and that the slow onset of effects is caused not by pharmacokinetic factors but by the time needed for mRNA and protein synthesis. The slow dissipation of steroid effects is governed by steroid elimination (time to decline below KD values), the KD for receptor binding, and the time required for mRNA and the TAT enzyme to readjust to baseline conditions. These studies provide insight concerning the integrated role of drug, receptors, and biologic response mediators in determining the role of dose, time, type of corticosteroid, and drug-disease interactions in governing the pharmacodynamics of these agents. The models are of more general value in pharmacology as well, for these cascade models should be relevant to the quantitation of any type of gene-mediated drug effect.