Although this “negative” finding may seem to contrast with previous studies on the role of endothelial cells in severe infection [16]–[20], our approach clearly differs from these earlier investigations, both with regard to the target of genetic manipulation (deletion of MyD88 versus inhibition of NFκB [16]–[19] and endothelial cell TLR4 expression on an otherwise TLR4 deficient background [20]) and the sepsis model used (pneumonia versus abdominal or intravenous infection [16]–[20]). This evidence concerns the gene MYD88 and susceptibility to pneumonia measurement.