Conversely, in a mouse model that overexpresses TNF-α and develops spontaneous RA-like lesions in the joints, deficiency of TNFR2, but not TNFR1, led to a more aggressive disease, with exacerbated synovial hyperplasia and enhanced destruction of bone and cartilage [32]. Here, TNFRSF1A is linked to rheumatoid arthritis.