The recent paper by Riddell et al (2002) was interesting and timely. However, the results were entirely predictable without any experimentation because of preselection of patients and the currently used definition of type 2M von Willebrand disease (VWD). Both the ristoctin cofactor (VWF:RCo) assay and the collagen-binding (VWF:CB) assay will be sensitive to loss of von Willebrand factor (VWF) protein and especially to the loss of the higher-molecular-weight (HMW) multimers. The current definition of type 2M VWD is ‘decreased platelet-dependent function that is not caused by the absence of HMW-VWF multimers’. Defects in the VWF glycoprotein Ib binding site will lead to loss of platelet-dependent function, cause type 2M VWD by this definition, and be detected by the VWF:RCo (but not the VWF:CB). Defects in the VWF collagen binding site will lead to loss of collagen-dependent function, cause a currently unclassified form of VWD, and be detected by the VWF:CB (but not the VWF:RCo). I suggest that ‘platelet-dependent’ is removed from the definition of type 2M VWD. Type 2M can then be subtyped as type 2Mp – decreased platelet-dependent function (the old 2M), or as type 2Mc – decreased collagen-dependent function. The VWF:RCo detects only the former and the VWF:CB only the latter. That type 2Mc exists is clear (Ribba et al, 2001). We will only know the relative importance of type 2Mp and type 2Mc when the VWF:CB is used as widely as the VWF:RCo.