(23) reported that mitochondrial dysfunction contributes to SLE pathogenesis, where the mechanism is a defect in the autophagic removal of the mitochondrial pathway during erythroid maturation, leading to the accumulation of red blood cells carrying mitochondria in SLE patients and the induction of IFN production through the activation of cGAS in macrophages. Here, IFNA1 is linked to systemic lupus erythematosus.