Studies have shown that inflammatory M1 macrophages of pancreatic cancer are stimulated by KrasG12D acinar cells, and release factors such as NF-κB and Notch that lead to improper activation of signal pathways to stimulate acinar to ductal metaplasia (ADM) and then undergo carcinogenesis (31, 32). This evidence concerns the gene NFKB1 and pancreatic neoplasm.