Overall, the data suggest that the JAK2-STAT1 pathway is profoundly disturbed in patients with sepsis caused by gram-negative bacteria, producing reduced levels of pSTAT1 after a second immune challenge with LPS and potentially leading to abnormal STAT dependent gene expression patterns that could drive the dysfunctional monocyte response in septic monocytes. The gene discussed is SOAT1; the disease is Sepsis.