These mice were treated with selective PI3K inhibitors improved renal function and lived longer than vehicle-treated controls.[41] In vitro experiments, indirubin was observed to restore the expression of PTEN on the CD4+ T cells of ITP patients, leading to the subsequent attenuation of the PI3K/AKT pathway and modulating the homeostasis of T cell.[26] It may be hypothesized that PI3K/Akt/mTOR pathway play a role in ITP and SLE initiation and progression. The gene discussed is CD4; the disease is autoimmune thrombocytopenic purpura.