Although FAO and glutamine metabolism might have a role in the activation of GVHD-inducing alloreactive T cells, elegant work has provided evidence that glycolysis is the dominant metabolic pathway of alloactivated donor T cells and inhibition of glycolysis by targeting HK-2 or the rate-limiting PFKFB3 prevents alloreactivity in vivo and attenuates GVHD in HSCT recipient mice (75). The gene discussed is HK2; the disease is graft versus host disease.