It is important to note that there may be overlap in DI-TMA and drug-induced or secondary TTP, wherein the latter is defined by a mechanistic association (ie, a severe acquired deficiency in, or inhibition of, ADAMTS13 activity), while DI-TMA is defined by a clinical association (ie, concurrent use of a drug) with mechanistic diversity (eg, autoimmunity, drug-dependent antibodies, or endothelial damage). This evidence concerns the gene ADAMTS13 and thrombotic thrombocytopenic purpura.