The invasiveness and metastasis functions of KITENIN were shown to be mediated by ERK/AP-1 activation through the interaction of KITENIN with Dvl/PKCδ [21] or the KITENIN/ErbB4-Dvl2-c-Jun axis, as an EGFR-independent EGF signal [23] in colon cancer cells. The gene discussed is JUN; the disease is colonic neoplasm.