Multiple dysregulated signaling pathways have been shown to be involved in ECM overproduction in keloids, such as the transforming growth factor β (TGF-β)/Smad, Wnt/β-catenin, phosphoinositide 3 kinase (PI3K)/AKT/mechanistic target of rapamycin (mTOR), and Notch-1/jagged canonical notch ligand 1 (JAG-1) pathways [1,7,8]. This evidence concerns the gene JAG1 and keloid.