These findings allowed us to further investigate the potential function of GPR65 on the differentiation of IBD CD4+ T cell, we then performed lentiviral transduction experiments in vitro and did find that LV‐GPR65 transduction IBD CD4+ T cells preferentially differentiated into Th1 and Th17 cells, while LV‐shGPR65 transduction CD4+ T cells displayed opposite effects. Here, CD4 is linked to inflammatory bowel disease.