These include effects on muscle atrophy/hypertrophy signalling, fibre shift, systemic inflammation and remodelling.31 Angiotensin II opposes the action of the insulin-like growth factor (IGF-1) system activating the ubiquitin-proteasome proteolytic pathway via IGF-1 and via NF-kB,32, 33 and IGF-1 levels are reduced in the quadriceps of COPD patients in the stable state compared to healthy controls.34 Increases in exercise capacity and fibre size in COPD patients undergoing PR are associated with upregulation of IGF-1 and its splice variant mechano-growth factor (MGF).35 Here, NFKB1 is linked to chronic obstructive pulmonary disease.