Using 4E-BP1/BP2 double knockout (DKO) mice and their wild-type (WT) littermates, we tested the hypothesis that deletion of 4E-BP1/BP2 would increase basal skeletal muscle protein synthesis and ameliorate the decrement in synthesis observed after induction of sepsis (a catabolic stressor), thereby demonstrating the central importance of eIF4E binding proteins in regulating muscle protein balance under in vivo conditions. Here, IGFBP2 is linked to Sepsis.