In addition, combined mutations in the Wnt/β-catenin and KRAS pathways synergistically amplify downstream signaling events, ultimately converging in the activation of the Jagged1 protein, with the release of functional fragments, the soluble Jag1-ECD, and the Jagged1 intracellular domain, which sustain malignant traits and tumor progression in CRC [21]. This evidence concerns the gene KRAS and neoplasm.