IFNA1 and systemic lupus erythematosus: Aberrant mitochondrial function is shown to be associated with SLE-fatigue which improved on reversal of mitochondrial oxidative stress by repletion of glutathione by administration of N-acetylcysteine.3 Mitochondrial dysfunction also led to dysregulation in the type I interferon (IFN) pathway thereby promoting immune dysregulation, suggesting a putative role in SLE-fatigue.4 5 These studies suggest a putative role of mitochondrial dysfunction in SLE-fatigue.