In animal experiments using KPC cells derived from KPC (LSL-Kras[G12D/+]; LSL-Trp53[R172H/+]; Pdx-1-Cre; a genetically engineered mouse model of PDAC) mice harboring KRAS and TP53 mutations, which was established as a model of human malignant PDAC, we observed that suppressing the expression of molecules constituting the ARF6-AMAP1 pathway had no effect on tumor formation in immunodeficient mice, but significantly suppressed tumor formation in syngeneic immunocompetent mice [352]. This evidence concerns the gene PDX1 and neoplasm.