IN recent years it has been recognized that autoantibodies to cell-surface receptors for hormones or neurohumoral agents can develop spontaneously and give rise to clinical states of altered endocrine or neuromuscular function. For example, autoantibodies to receptors for acetylcholine in skeletal muscle are associated with myasthenia gravis, those to receptors for thyroid-stimulating hormone are associated with Graves' disease, and those to receptors for insulin in patients are associated with certain forms of insulinresistant diabetes, such as the one involved in acanthosis nigricans.1 These autoantibodies may either mimic or inhibit hormone action, depending on the tissue, the receptor, and perhaps even . . .