THE weakness and fatiguability of skeletal muscle in rayasthenia gravis (MG) is thought to be due to interference with neuromuscular transmission that follows binding of antibody to acetylcholine receptors (AChRs). Anti-AChR antibody is present in 85 to 90 per cent of patients with generalized MG (Mittag, Kornfeld, Tormay and Woo, 1976; Lindstrom, Seybold, Lennon, Whittingham and Duane, 1976). MG immunoglobulin can passively transfer MG to the mouse (Toyka, Drachman, Griffin, Pestronk, Winkelstein, Fischbeck and Kao, 1977) and anti-AChR antibody is present in infants with neonatal MG through placental transfer from myasthenic mothers (Keesey, Lindstrom, Cokely and Hermann, 1977). Plasma exchange, which lowers serum antibody, is associated with clinical remission (Pinching, Peters and Newsom-Davis, 1976) and reveals an inverse relation between muscle strength and serum antibody levels (Dau, Lindstrom, Cassel, Denys, Shev and Spitter, 1977; Newsom-Davis, Pinching, Vincent and Wilson, 1978). The number of functioning AChRs is reduced in MG (Fambrough, Drachman and Satyamurti, 1973) and the reduction is adequate to account for the physiological abnormalities (Ito, Miledi, Vincent and Newsom-Davis, 1978). The antibody appears to exert its effect by several mechanisms including complement mediated lysis of the post-synaptic membrane (Engel, Lambert and Howard, 1977), increased rate of degradation of acetylcholine receptor (Stanley and Drachman, 1978) and possibly by direct pharmacological block (Shibuya, Kazutake and Nakazawa, 1978).