The hypothesis that a global defect in cellular calcium transport may be critical in the development of familial benign hypercalcaemia (FBH) was investigated. Nine hypercalcaemic patients from a kindred with FBH and nine normal subjects were evaluated. Our results indicate that calcium pump activity in the FBH kindred was significantly higher (28%, P < 0.005) when compared to normal subjects. These findings suggest that alterations in calcium pump activity in target tissues may play a role in the development of FBH.