It has been long established that VWF–GPIbα catch-bond behavior well correlates with the counterintuitive high shear-dependent and shear-enhanced platelet adhesion to the VWF surface.34,64,68,69 Conversion of VWF–GPIbα catch bonds to slip bonds was shown to associate with von Willebrand disease mutations.1,18,19 Our results further demonstrated that the long N-AIM sequence in VWF-A1 (i.e., 1238-A1) stabilized the catch-bond behavior, while truncating the N-AIM (i.e., 1261-A1) altered the binding kinetics and resulted in the bi-variable catch-to-slip bond phenotypes. This evidence concerns the gene VWF and Von Willebrand disease.