During the development of IBD, MLCK‐mediated phosphorylation of MLC2 leads to TJ disruption and intestinal mucosal barrier damage.[48, 49] This is consistent with our findings, where we observed that overexpression of SPARC promoted protein expression of p‐p65, MLCK, and p‐MLC2 in vitro and in vivo. Here, SPARC is linked to inflammatory bowel disease.