We speculate that in our system, upregulation of Slc7a11 in cells stimulated with LPS might represent a compensatory mechanism triggered to counter the early redox stress generated in the setting of endotoxemia, or perhaps upregulation of Slc7a11 promotes disruption of other critical pathways, thereby leading to tissue injury, but this requires further investigation. This evidence concerns the gene SLC7A11 and serum lipopolysaccharide activity.