In contrast, Emf6.1Fab/EMA601 completely blocked hGPVI-mediated activation and coagulant activity in vitro and ex vivo, thus confirming the central role of GPVI in this process.20 This translated into strong protection of hGP6tg/tg mice from arterial thrombosis while not affecting tail bleeding time, confirming that a complete loss of GPVI-mediated platelet activation is not associated with increased bleeding. The gene discussed is GP6; the disease is Arterial thrombosis.