Minimal change nephrotic syndrome has been proposed to be a disorder of T cell dysfunction. It is hypothesized that a circulating factor(s) from activated T cells might alter glomerular permeability to protein. Some studies have provided evidence that up-regulation of interleukin-2 may be involved, not only in the pathophysiology of minimal change nephrotic syndrome, but also in steroid resistance. Basiliximab, an anti-interleukin-2 receptor antibody, is indicated for the prophylaxis of acute organ rejection in adults and children with kidney transplants. Clinical trials have shown that basiliximab is effective and well tolerated. We describe here a pediatric patient who continuously had massive proteinuria and hypoalbuminemia for 5 years, despite pulse therapy with methylprednisolone and cyclophosphamide and prolonged oral treatment with cyclosporine and mizoribine. He had experienced several disease- and treatment-associated complications, such as bacterial infections, indirect inguinal hernias, and cataracts. After he had been given a single dose of basiliximab, he achieved complete remission of proteinuria and then discontinued all immunosuppressant treatment.