My recent review, which focused on the role of SOCS in human RA [30], indicated that the resultant hyperplastic synovial tissue characteristic of RA is comprised of a host of activated immune cell types, including T- and B-lymphocytes as well as macrophages, dendritic cells, mast cells, neutrophils and fibroblast-like synoviocytes (FLS), all of which appear to be “apoptosis-resistant” [44], whereas the frequency of apoptotic chondrocytes is elevated, thus potentially reducing chondrocyte vitality and viability [30,44]. The gene discussed is CISH; the disease is rheumatoid arthritis.