And finally, there is a family with a mutation in the heparin sulfate 3-0-sulfatransferase-6 gene that leads to HAE where there are two unproven assumptions: (A) that it leads to overproduction of bradykinin – this seems likely to be proven correct, and (B) the mutation diminishes sulfation of cell surface proteoglycan (60), but instead of decreasing bradykinin production, it leads to the opposite effect. Here, KNG1 is linked to hereditary angioedema.