First, ASK1 is kept inactive under normal physiological conditions through binding to the reduced form of thioredoxin and only undergoes auto‐activation upon the oxidation and dissociation of thioredoxin during pathological oxidative stress—an important feature in many forms of kidney disease.3, 22 Second, mice lacking the Ask1 gene have a normal phenotype consistent with a lack of involvement of ASK1 in normal physiology.3, 22 Third, p38 and JNK are the only known downstream targets of ASK1 activation thereby providing a potentially selective means to target these pathways.3, 22. This evidence concerns the gene TXN and kidney disorder.