In line with the present results, functional studies of some type 2A variants have shown that this VWD type arises from multiple mechanisms, including intracellular retention or degradation of VWF, defective multimerization, impaired regulated storage, and increased proteolysis, with several variants exhibiting overlapping defects in both intracellular and extracellular processes [51]. This evidence concerns the gene VWF and von Willebrand disease (hereditary or acquired).