Such findings are consistent with pre-clinical mouse studies, in which depleting isotypes of anti-GITR and anti-OX40 demonstrated maximal anti-tumor activity in vivo, associated with their ability to enhance effector function with concomitant depletion of tumor-infiltrating Treg cells (Bulliard et al., 2014, Coe et al., 2010). The gene discussed is TNFRSF4; the disease is neoplasm.