Abstract Injection of a hyperphysiological dose of 17β-estradiol to the rat elicits a translocation of the cytoplasmic estrogen receptor in the kidney. This is followed, a few hours later, by an increase in the rate of ornithine aminotransferase synthesis. This increase, in turn, causes the enzyme activity to rise also a few hours later. Growth of rat kidney tumor MK3 has delayed the induction of ornithine aminotransterase by 17β-estradiol in the host kidney. However, the enzyme is not inducible in several normal tissues where the activity is high and where concentrations of estrogen receptor greatly exceed that in rat kidney. These observations suggest certain possible mechanisms of the inductive process.