Given the current data showing an upregulation of CHOP expression at later ages and in disuse atrophy, an increased nuclear localization of CHOP following HLI, and the upregulation of known downstream genes affected by CHOP with HLI, we posit that CHOP could play a key role in aging- and disuse-induced skeletal muscle atrophy. This evidence concerns the gene DDIT3 and muscle atrophy.