As Tregs constitutively express OX40, and Ox40-Cre–mediated deletion of Brd4 in Tregs compromised their suppressive functions, this Treg defect in Brd4fl/fl Ox40-Cre mice allowed hyperactivation of γδ T cells in situ, thus further contributing to the development of dermatitis and hair follicle destruction. The gene discussed is TNFRSF4; the disease is skin disorder.