Both pro-inflammatory innate (e.g., dendritic cells [DCs], macrophages, and neutrophils) and adaptive (e.g., T helper [Th]1, Th17, CD8 T, and B) cells, which can organize into discrete lymphoid aggregates with germinal centers in RA, are strongly involved in initiating and maintaining the disease through the production of autoantibodies and many cytokines that act both in series and in parallel, meaning cascades of action and redundancy [1,2,9–14]. Here, CD8A is linked to rheumatoid arthritis.