However, there are many poorly understood features in NE pathobiology such as (i) the role of galectin-3-binding protein, the levels of which correlate with increased complement activation and with clinical variables reflecting the severity of acute hantavirus infection [24], (ii) the mechanism of thrombocytopenia [25], (iii) neutrophil activation [26], and (iv) interferon-dependent induction of tissue plasminogen activator (tPA) both in cultures of endothelial cells and in vivo in NE patients [27]. This evidence concerns the gene PLAT and hantavirus infectious disease.