SIRT6 supports the switch from hyper- to hypo-inflammatory response in sepsis inflammation by countering NFĸB p65 and HIF1-α-dependent glycolysis during hyper-inflammation, while SIRT1 couples to PGC-1 to increase fatty acid oxidation as hypo-inflammation and endotoxin tolerance develop; specifically, SIRT1 and SIRT6 coordinate the immunometabolic switch during sepsis [7]. Here, PPARGC1A is linked to Sepsis.