There is currently great interest in the targeted therapy of cancer. Antibodies that target specific antigens on the surface of cancer cells — such as rituximab, which binds to CD20 on lymphoid tumors, and trastuzumab, which blocks HER2 on breast-cancer cells — were early successes. However, a novel method of using antibodies to stimulate an antitumor response was pioneered in the mid-1990s by James Allison and colleagues.¹ Because the body's immune response, if left unchecked, can result in autoimmunity, we have evolved a number of immune “checkpoints” that work as braking mechanisms to counterbalance immune activation. Studies in animals have . . .