These latter data are consistent with preserved IFN-γ and IL-17 production observed in AMPKa1–/– T cells during viral infections (26) and together suggest that improvements in GVHD following transplantation of AMPK-dKO T cells are not driven by changes in the canonical AMPK-related pathways of fat oxidation, autophagy, or mTOR signaling. The gene discussed is PRKAA1; the disease is viral infectious disease.