Rapamycin inhibits the mTOR pathway by increasing both the number of regulatory T cells and the production of IL-2, a cytokine essential for regulatory T cells.[1] Activation of mTOR is thought to be a major cause of TSC and is associated with mutations in TSC1 and TSC2, thus implying a relationship between SLE and TSC. This evidence concerns the gene TSC2 and tuberous sclerosis.