glutaminolysis, [48]. In addition to promoting energy production, AMPK inhibits processes that consume energy. For example, AMPK phosphorylates acetyl-CoA carboxylase 1

(ACC1) to inhibit fatty acid biosynthesis [49]. AMPK also inhibits mTOR activity to limit protein synthesis via phosphorylation of tuberous sclerosis complex 2 (TSC2) [50] and

Raptor [51]. At least in part due to its ability to regulate metabolic switches in response to

glucose deprivation, especially the upregulation of fatty acid oxidation and restraint of

mTORC1 activity, AMPK also plays an essential role in CD8+ T cell memory formation [52, 53].Altogether, studies on mTOR and AMPK and other metabolic regulators over the past decade highlight the notion that T cell metabolism is not merely a downstream effect of T

cell activation and differentiation, but rather it can actively participate in the instruction of