Among them, it has been proved that the EGF-like domains present in MUC4 interact with ErbB2 and ErbB3 receptors to trigger intrinsic protein–tyrosine kinase activity and further activate intracellular signaling pathways (e.g., mitogen-activated protein kinase [MAPK], phosphatidylinositol-3-kinase [PI3K]–Akt, protein kinase C [PKC] pathways), and coactivate transcription of the downstream effector molecules to mediate malignant functions of tumor, including pancratic cancer [15, 16, 26–30]. Here, MUC4 is linked to neoplasm.