Administration of 17\g=a\-ethyl-19-nortestosterone(50-100 mg/day) to four men with peptic ulcers caused a reduction in the excretion of 17-ketosteroids and 17-ketogenic steroids. All the major urinary 17-ketosteroids were decreased by this treatment, but 11\g=b\-hydroxyandrosterone appeared to be least affected.Single injections of androst-4-ene-3:17-dione were given to one patient both before and during the period of ethyl-nortestosterone treatment. Recovery of the metabolites of androstenedione in the 48 hr following injection was virtually the same in the pretreatment and treatment periods. This was interpreted to mean that alteration of the metabolism of this adrenal steroid was not the basis of the suppression of ketosteroid excretion.It is therefore concluded that 17\g=a\-ethyl-19-nortestosterone can cause suppression of adreno\x=req-\ cortical secretion.Ingle & Mason [1938] first demonstrated atrophy of the adrenal cortices of rats into which pellets of cortisone had been implanted. Since then many workers have found a depression of urinary 17-ketosteroid (17-KS) excretion in human individuals to whom cortisone has been administered. Recently a number of synthetic compounds, which possess some physiological properties similar to those of cortisone, have been shown to depress urinary 17-KS excretion. These include prednisone, prednisolone and their 9«-fluoro derivatives.There have also been reports of an adrenal-depressing action exerted by steroids more distantly related to the corticoids. Hoagland [1944] reported that pregnenolone injected intramuscularly in doses of 50-150 mg/day caused depression of urinary 17-KS. Partridge, Boling, De Wind, Margen & Kinsell [1953] found that androstenediol (1 g/day) caused a reduction of the 17-Carroll [1945] reported that administration of methyltestosterone caused a decrease in the urinary excretion of 17-KS of seven patients. One of those patients was a man with congenital absence of functioning testicular tissue and the remaining six were women. They also found a suggestive, but not conclusive, decrease in the 17-KS of two male patients with Addison's disease. Bartter, Forbes, Jefferies, Carroll & Albright [1949] established that methyltestosterone and testosterone propionate produced a fall in 17-KS and '11 oxysteroids' in certain females with Cushing's syndrome.The purpose of this paper is to describe some effects of 17 -ethyl-19-nortestosterone