Urinary 17-ketosteroids or their precursors are thought to arise from the adrenal cortices and the testes (1). Testosterone propionate is partially excreted as a 17-ketosteroid (2); on the other hand, 17-methyl testosterone is not excreted as such (3 to. 5). It follows that methyl testosterone in contradistinction to testosterone propionate, may be used to study the effect of a testosterone compound on the endogenous production of urinary 17-ketosteroids. The present paper is primarily concerned with the effect of methyl testosterone on the urinary 17-ketosteroids of adrenal origin.It is essential that such studies be carried out on individuals without functioning testicular tissue, since it is highly probable from animal experiments that testosterone inhibits its own endogenous production in the testis (6 to 8). It is difficult to obtain direct data in humans on the effect of testosterone on the urinary 17-ketosteroids of testicular origin. Thus, whereas the administration of methyl testosterone to a male without disease of the adrenals and testes induced a lowered 17-ketosteroid excretion (Figure 1), the entire effect may have been mediated through