The cellular mechanism responsible for the sepsis-induced decrease in skeletal muscle protein synthesis results at least in part from impaired kinase activity of mTOR (mammalian target of rapamycin), as evidenced by the reduced phosphorylation of two down-stream substrates – eukaryotic initiation factor (eIF) 4E binding protein (4E-BP1) and the 70 kDa ribosomal protein S6 kinase (S6K)-1 [8], [12], [13]. This evidence concerns the gene MTOR and Sepsis.