Some of the targets for such an approach can be β-catenin molecules in tumour cells, IL-6, and related TLRs in areas of severe inflammation and microbiota dysbiosis in the body; molecules like E-cadherin and Gal–GalNac that are overexpressed on tumour cells and act as binding sites for bacteria or their effector molecules; and miRNAs involved in the autophagy of tumour cells and their increased proliferation. The gene discussed is CDH1; the disease is neoplasm.