The expectation of survival of skin homografts in a strain of albino rats has been compared with that of ovarian homografts made subcutaneously in ovariectomized recipients. It was found that a degree of genetic—and therefore antigenic—difference between donor and host that will lead to the breakdown of skin homografts is only rarely sufficient to affect the continued functional activity of ovarian homografts. Ovarian homografts implanted into ovariectomized recipients which had previously received skin homografts from the same donor failed to survive in nearly all those animals which had reacted vigorously against their skin homografts. It seems, therefore, that the majority of ovarian homografts are themselves incapable of provoking reactions, but are not exempt from the immunity elicited by previous homografts of the donor’s skin. Thus skin and ovary share at least some antigens in common. The most likely reasons why ovarian homografts are more successful than skin homografts are (1) that ovarian tissue is characterized by fewer genetically defined ‘histocompatibility' antigens than skin, and (2) that the ‘histocompatibility’ antigens of ovarian tissue are feeble, being capable of eliciting only a weak immune response, if any.