Indeed, the synovium of patients with rheumatoid arthritis and the affected skin of scleroderma patients exhibited increased activation of mTOR compared to osteoarthritis, or the normal skin, respectively, whereas the administration of rapamycin, an Akt/mTOR pathway inhibitor, in lupus patients and experimental models lowered the proinflammatory T-cell subsets by reverting the expansion of Th17 and upregulating Tregs [23,24,25,26,27,28]. The gene discussed is AKT1; the disease is rheumatoid arthritis.