Different from its first identified target IGF2 under normal skeletal muscle growth, we conclude that DOCK3 is the main target of ZBED6 under conditions of sepsis‐induced muscle atrophy based on the evidence that 1) integrated analysis of RNA‐seq in nine depots of skeletal muscles from septic ZBED6−/− pigs and WT controls and ZBED6 ChiP‐seq in pig muscle tissue converged on DOCK3, 2) direct binding of ZBED6 on the promoter region of DOCK3, and 3) cellular phenotype that knockdown of DOCK3 abolished the protective role of ZBED6 deficiency on sepsis‐induced muscle atrophy. This evidence concerns the gene IGF2 and Sepsis.