MLCK is a component of the actin cytoskeleton[26] and NF‐κB p65‐induced MLCK/MLC2 pathway activation participated in the modulation of intestinal barrier disruption.[27] Hence, we inferred that SPARC contributed to intestinal epithelial barrier dysfunction in CD by regulating the OTUD4/MYD88/NF‐κB/MLCK/MLC2 pathway. This evidence concerns the gene SPARC and Cowden disease.