Although the reports mentioned above found no genetic variations in ERCC2/XPD or ERCC5/XPG when they were linked to SLE, the observed mitochondrial dysfunction in SLE, which implicates ATP depletion [20,21], combined with the underexpression of ATP-dependent ERCC genes suggests impaired DNA repair or consequently increased apoptosis, both of which may contribute the clinical or laboratory manifestations of SLE. This evidence concerns the gene ERCC5 and systemic lupus erythematosus.