They did not find evidence that the antibodies were directed against ADAMTS13, loss of which contributes to a related thrombotic microangiopathy (see below), and instead hypothesized that the antibodies were against Stx itself and were crosslinking receptors, causing the release of larger von Willebrand Factor multimers [77] to indirectly inhibit ADAMTS13 [65] and increasing risk of thrombus formation. This evidence concerns the gene ADAMTS13 and thrombotic microangiopathy.