Rapamycin treatment restored normal levels of mTORC1 activation, lessened the severity of cytopenia, hyperferritinemia, and hepatosplenomegaly (Fig. 6a–g), and downregulated the production of IFN-γ, an important cytokine in the pathogenesis of MAS (Fig. 6h). The gene discussed is IFNG; the disease is isolated hyperferritinemia.