We have demonstrated that ABCB1 inhibition depletes cells of Gb3 by preventing its de novo synthesis, and that Fabry mice treated by enzyme replacement therapy followed by administration of cyclosporine A, an ABCB1 inhibitor, failed to accumulate Gb3 in the liver, suggesting that inhibition of ABCB1 may have therapeutic consequences for Fabry disease patients [26]. The gene discussed is ABCB1; the disease is Fabry disease.