Recent reports showed that the MT membrane potential and the proliferation inhibition function of CD4+Foxp3+ Treg from patients with myasthenia gravis are enhanced by autophagy inducing agent rapamycin and suppressed by phosphoinositide 3-kinase (PI3 kinase) and autophagy inhibitor 3-methyladenine (3-MA) (102) and that during autoimmune conditions, Treg function alterations associate with MT oxidative stress, dysfunctional mitophagy, and enhanced DNA damage and cell death (103, 104). The gene discussed is FOXP3; the disease is myasthenia gravis.