Validation of MLC phosphorylation in controlling TJ-mediated solute permeability was initially validated using a rationally designed, stable, membrane permeable inhibitor of MLC kinase (PIK) peptide that was shown to be effective in models of chronic epithelial inflammation where unabated MLC kinase (MLCK) activity maintains the epithelia in a hyper-permeable state characterized by increased pMLC levels [12,39]. This evidence concerns the gene MLC1 and inflammatory response.