Engineering of the IgG1 Fc region for enhanced and/or specific binding to FcγRIIb can greatly improve agonistic function.72, 118, 119, 120 Such mutations induced significantly greater agonistic activity in an anti‐DR5 model through increased induction of apoptotic death and decreased tumor growth compared with unmodified IgG1.121 The “SELF” modifications that dramatically and selectively increase affinity for FcγRIIb have also been used to enhance immune agonism in an anti‐OX40 model.122