Complement proteins are abundant in the immune microenvironment [9] and emerging evidence indicates that the pathological activation of the complement system in the TME triggers tumorigenesis by regulating the inflammatory response and immunosuppressive stromal cells in the TME, thereby promoting the epithelial–mesenchymal transition (EMT), proliferation, migration, and tumor metastasis in various cancer types [23,24,25]. This evidence concerns the gene VTN and cancer.