However, one recent study shows that the cytokine and colitis-inducing potential of Th9 is controlled by CD96 expression: adoptive transfer of CD96low Th9 into Rag1−/− mice induces severe intestinal inflammation, while transfer of CD96high Th9 does not cause colitis and blockade of CD96 can restore the expansion and inflammatory properties of CD96high Th9 cells [160], which indicates a functional heterogenicity of Th9 cells. Here, CD96 is linked to colitis.