Inhibition of this ATPase leads to mitochondrial hyperpolarization and ATP depletion, features similar to those observed in SLE, but in vivo treatment of MRL/lpr mice with Bz-423, an inhibitor of mitochondrial F1F0 ATP synthase, leads to apoptosis of autoreactive CD4+ T cells and suppression of glomerulonephritis [17]. The gene discussed is CD4; the disease is systemic lupus erythematosus.