Evidence from in vitro experiments also demonstrated that claudin-3 is downregulated by proinflammatory cytokines (e.g., IFN-γ, TNF-α, and IL-1β)-induced myosin light chain kinase (MLCK) activation (97, 98).In claudin-3-deficient mice model, colonic epithelial dedifferentiation, barrier dysfunction and rapid tumor progression likely resulted from IL-6/gp130/STAT3 signaling-induced Wnt/β-catenin signaling upregulation, indicating the interaction between inflammation and tumorigenesis mediated by claudin-3 deficiency (69). This evidence concerns the gene CLDN3 and neoplasm.