We observed that host glucosetransporter GLUT1 expression was substantially diminished in the infectedlesions of Rapa-treated mice during peak infection (Fig. 7A and B), similar to the extent to which GLUT1 isabsent in the lesions of phagocyte-specific GLUT1 knock-out mice (LysM-CreGLUT1fl/fl mice; Fig. 7C andD). The gene discussed is SLC2A1; the disease is infection.