These results are consistent with UC patients and our previous data showing a significant reduction in ZO-1 expression in DSS colitis-induced mice35 due to RACK1 deficiency-related SRC activation76,77 that was restored by a TAT–GILZ pharmacological strategy.35 Therefore, our data highlight that RACK1-related GILZ expression is critical for sequestering SRC and preventing epithelial barrier dysfunction in colitis, thus contributing to the understanding of how to improve therapies. Here, TSC22D3 is linked to colitis.