There is not even a suggestion here that human heart disease involves this gene, or an excess of GSH. In fact, when the redox balance is tested in human heart disease, there is usually, or always, oxidative stress. Mice, unlike humans, make their own vitamin C, lots of it, which has to make a difference.

Homocysteine is the rogue antioxidant in human heart disease, reducing poorly liganded copper and iron, which then generate oxidative stress and neutralise nitric oxide, NO, to ONOO. This constricts blood vessels and oxidises cholesterol.