MYLK and inflammatory bowel disease: This phosphorylation triggers a contractile force that increases physical tension on tight junctions, potentially causing structural deformations and thereby elevating paracellular permeability.76 Enhanced expression and activity of MLCK are frequently observed in cases of IBDs in both rodent models and human patients, making it an attractive therapeutic target.77,78 Several recent studies have explored the potential of MLCK inhibition in controlling IBD pathology and reducing intestinal permeability.79,80