OESTROGENS are more readily accumulated and retained in responsive cells than in cells that are not their targets¹. Cytoplasmic macromolecules² which specifically interact with oestradiol and other steroid hormones seem to mediate transfer of the agonist to the nuclear chromatin, where the complex is believed to promote expression of the phenotypic effects^3–6. It is generally assumed that the hormone diffuses passively to “cytoplasmic” receptors which determine the cellular specificity of response⁷. But some experiments indicate that steroid hormones interact with components of biological membranes and may enter their respective target cells by a membrane-mediated process^8–12 which is saturable and temperature-dependent^13–17. We have investigated steroid-binding components associated with the plasma membranes of cells isolated from endometrium, liver and intestinal mucosa. Endometrial and liver cells show substantial binding to oestrogen immobilised by covalent linkage to an inert support, while intestinal cells have no such binding sites. The relative quantity of these steroid receptors at the outer surfaces of cells from diverse tissues corresponds well with the capacity of a given cell to accumulate and retain oestrogen.