Tim-3 can be shed from the cell surface by a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13) or ADAMTS17-mediated cleavage of the TIM-3 stalk region, resulting in a soluble from that is elevated in the sera of patients with autoimmune diseases [7, 8]. This evidence concerns the gene HAVCR2 and autoimmune disease.