THE molecular basis of the many effects of 5,5-diphenylhydantoin (DPH, Dilantin) remains obscure. In addition to being the drug of choice in the prevention of seizures1, DPH is used to correct cardiac arrhythmias (mainly those caused by digitalis)2, and to control myokymia (continuous muscle fibre activity)3, and excessive secretion of insulin4 or anti-diuretic hormone5. Side effects include hypotension, hyperglycaemia and disturbances of calcium homeostasis6. Among the actions proposed for DPH are stimulation of active sodium/potassium transport7, inhibition of passive sodium influx in stimulated (but not in resting) cells8,9, reduction of calcium influx10,11, and specific interference with synaptic transmitter movements12. We report here that DPH does not affect active sodium transport, but blocks passive resting sodium channels in much the same way as tetrodotoxin (TTX) does, and we suggest that from this elementary action may follow many of the drug's therapeutic, adverse, and in vitro effects.