The mechanisms responsible for skeletal muscle dysfunction in COPD remain a matter of controversy and are likely multifactorial, but there is evidence that chronic activation of the IM renin-angiotensin system may be a key pathophysiologic pathway.8 In animal models,9‐11 angiotensin II promotes muscle loss via an inhibitory effect on the insulin-like growth factor (IGF)-1 system and stimulation of a catabolic pathway mediated by two ubiquitin ligases, the atrogenes: muscle RING finger protein-1 and atrogin-1. Here, AGT is linked to chronic obstructive pulmonary disease.