Additionally, in our patients, the increased PT, as well as its positive correlation with u-CysLT—which also exhibited several positive correlations with inflammation and endothelial markers—is suggestive of u-CysLT’s contribution to intravascular coagulation, which is also a documented promotor of organ injury in sepsis both via endotoxin, as in the case of the majority of our urosepsis patients, or via cytokines like TNF, through induction of tissue-factor expression on monocytes and activated endothelial cells [104]. The gene discussed is TNF; the disease is Sepsis.