Notably, patients with type 2A VWD, reflecting loss of HMWM VWF plus possible defects in VWF activity (according to genetic variant may express both defective GPIb and collagen binding), and are reported to have a more severe bleeding phenotype than patients with 2M VWD (who often reflect a loss of GPIb binding, but potentially normal collagen binding, and who do not suffer from loss of HMW VWF) [[29], [30], [31], [32], [33]]. The gene discussed is VWF; the disease is von Willebrand disease (hereditary or acquired).