All mice in our study were C57BL/6J (not N), but it would be intriguing to interrogate the reduced ability to clear free radical damage, spontaneous oxidation of NADPH, and altered GSH:GSSG ratios in the tissues of mice with the NNT mutation, and further determine if targeting NNT (as has been done in a mouse model of polycystic kidney disease [51]) could be useful in future models of sepsis. This evidence concerns the gene NNT and polycystic kidney disease.