The pathology of this syndrome is the deficiency of ADAMTS13 enzyme activity, which could be inherited from congenital conditions due to hundreds of gene mutations or acquired by forming ADAMTS13 antibodies known as immune TTP or iTTP, which reduces the ability to prevent the blood accumulation of platelet-hyper adhesive ultra-large von Willebrand factor (VWF) multimers, leading to the development of clots composed primarily of platelets in the microvasculature [1]. This evidence concerns the gene VWF and thrombotic thrombocytopenic purpura.