These might include the development of lymphadenopathy of MRL-lpr mice, the generation of CD4–CD8– TCR-αβ+ T cells and the production of autoantibodies, which may result from the absence of cell death occurring during homeostatic proliferation of lymphocytes.17 48 Consequently, the upregulation of genes during T-cell homeostatic proliferation involved with cytolysis and inflammation, such as granzyme B, perforin and Fas-ligand,22 is likely to still contribute to inflammation during MitoQ therapy. This evidence concerns the gene CD8A and Lymphadenopathy.