Studies on the therapeutic efficacy of PRI-724/ICG-001 in pancreatic cancer have revealed one potential mechanism that Wnt/β-catenin-dependent inhibition of cell proliferation was partially due to downregulation of various genes that are involved in cell cycle, e.g. CCNE1, E2, and A2 [59, 62]. Here, CCNE1 is linked to pancreatic neoplasm.