A little over a decade ago, we reviewed studies on the role of T cells in rheumatoid arthritis (RA) and concluded that the prevailing paradigm was not consistent with the data (1). At the time, the primacy of T cells in the pathogenesis of autoimmune disease was undisputed. Based on a series of studies demonstrating a surprising paucity of T cell cytokines in the joints of our patients and the dominance of macrophage and fibroblast products (2–4), we proposed that the perpetuation of RA was not necessarily an antigen-specific process and that T cells were only one of several important players. Recently, the potential role of T cells in the pathogenesis of RA was reviewed, and their ambiguous contribution was emphasized (5). Now, 12 years later, we think it reasonable to revisit these issues. It is important, though, to frame the questions appropriately. Our original hypothesis did not suggest that T cell products were absent from the rheumatoid joint. Rather, we argued that the presence or absence of T cell products in the joint is not as important as their relative amounts in RA compared with known antigen-specific T cell–mediated disease. Indeed, after several years of debate, the notion that T cell cytokines are relatively low (but not absent!) in RA is now ingrained in the literature (6, 7). Moreover, it is apparent that viewing RA as simply a T cell–mediated or T cell–independent disease is a narrow perspective. Our original hypothesis needs to be placed in a larger context. RA could be considered as three separate, albeit interrelated, processes: disease initiation, perpetuation, and terminal destruction. In addition, we propose that antigen-independent mechanisms might play an integral role during all stages of RA.