These results reveal that the abundance of DN T cells is controlled by two different mechanisms in SLE: i) expansion via Rab4A-dependent mTOR activation as noted in B6.TC/Rab4AQ72L mice; and ii) contraction via Rab4A-independent mTOR activation in B6.TC/Rab4AQ72L-KO mice, both of which can be reversed by treatment with rapamycin. The gene discussed is RAB4A; the disease is systemic lupus erythematosus.