The initial presence and the subsequent recurrence of an extra-skeletal squamous cell carcinoma of the lung were associated with hypercalcaemia and hypophosphataemia unaffected by large dosages of prednisone or oral Na2HPO4 but responsive to buffered phosphate administered intravenously. An extract of the tumour produced hyperphosphaturia by blockade of tubular reabsorption of filtered phosphate. Though the phosphaturic action of the extract indicated the presence of a parathyroid hormone-like molecule in the tumour, the patient's parathyroid glands were enlarged at necropsy. The latter finding raises the possibility that the tumour may have been elaborating both a parathyroid hormone-like principle and a parathyrotrophic principle. At present there are no data which support the thesis that cancers can elaborate a principle which stimulates the parathyroid glands in terms comparable to ACTH, TSH, etc. It is more likely that in our patient the phosphate loads administered in attempts to reduce the hypercalcaemia were responsible for the parathyroid hyperplasia.