Experimental evidence accumulated to date shows that gC1qR can interact with various molecules in the tumor cell environment, including proteins of the kinin system such as factor XII and high-molecular-weight kininogen (HK), thereby triggering activation of the kinin–kallikrein system (KKS) resulting in the generation of bradykinin—one of the most potent vasoactive peptides known78. This evidence concerns the gene C1QBP and neoplasm.