Nevertheless, metabolic abnormalities have been reported in CD8+ T cells in adult-onset SLE and have been attributed both to prolonged type I IFN exposure and T cell receptor (TCR) stimulation and also to mitophagy inhibition through CD38 expression leading to reduction in CD8+ T cell cytotoxicity and altering the function and morphology of mitochondria in adult-onset SLE [23, 32, 33]. The gene discussed is CD38; the disease is systemic lupus erythematosus.