RACK1 and colitis: 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.