PTC overexpressing claudin-1 showed a more aggressive clinical course; however, claudin-1 expression appeared to be independent of the Wnt/β-catenin pathway, through which claudin-1 increased the susceptibility to colitis-associated cancers by increasing Wnt/β-CatSer552 signaling in Notch/PI3K/Akt-dependent manner [21,22]. This evidence concerns the gene AKT1 and cancer.