SCN10A and Sepsis: As mentioned above, early mortality in Nav1.8-Cre Rosa26DTA nociceptor-deficient mice during LPS-induced shock has been attributed to increased brain QUIN levels, and mortality in these mice is ameliorated by the central administration of an IDO1 inhibitor, suggesting that the peripheral influx of QUIN and other KYN metabolites into the brain during sepsis has a negligible effect on survival [5] (Figure 2).