As Treg cells can downregulate Foxp3 and become effector cells under certain conditions (Komatsu et al, 2014), it is possible that NR4A2‐dependent pathogenic Th cells with high‐affinity TcR for self‐antigens may be converted from common Treg precursor in the peripheral pool or switch directly from Treg cells during autoimmune disease development. The gene discussed is NR4A2; the disease is autoimmune disease.