Initially, gut microbial and metabolite-induced inflammation perpetually enables the development of pancreatic cancer, as has been reported in animal models, and LPS generated from Gram-negative bacteria can act through TLR4 to enable the activation of proinflammatory NF-κB and mitogen-activated protein kinase signaling, thus facilitating pancreatic carcinogenesis.359 Furthermore, the accumulation of certain intestinal and intrapancreatic bacteria fosters a tolerogenic immunosuppressive microenvironment conducive to cancer development and resistance to immunotherapy. This evidence concerns the gene NFKB1 and cancer.