Conversely, treatment of Tregs obtained from these patients with an mTOR inhibitor restores their suppressive function.8 In Foxp3-deficient murine Treg cells, the regulatory function can be re-established by specifically deleting the mTORC2 adapter gene Rictor but not by deleting the mTORC1 adaptor gene Rptor. 8 Moreover, deletion of Foxo1, the expression of which is reduced due to hyperactivation in Foxp3-mutated Tregs, impairs the reversal of IPEX syndrome in mTORC2 KO mice. Here, FOXP3 is linked to immune dysregulation-polyendocrinopathy-enteropathy-X-linked syndrome.