HAVCR2 and rheumatoid arthritis: TIM-3 can be shed from the cell surface via a disintegrin and metalloproteinase with thrombospondin motifs 10-mediated or ADAM 17-mediated cleavage at the TIM-3 stalk region, resulting in a soluble form of T cell immunoglobulin domain and mucin-3 (sTIM-3) that can be detected in serum.[13] We hypothesized that the TIM-3 axis is dysregulated in RA, and may be involved in rheumatoid inflammatory processes.