This idea is supported by the finding that in mice with chronic kidney failure, pharmacological inhibition of MSTN blocks muscle atrophy,109 and that pharmacological inhibition of the ActII‐receptor, which mediates MSTN signalling, prevents glucocorticoid‐induced muscle atrophy.110In vitro, glutamine reduced the tumour necrosis factor alpha‐dependent increase of MSTN.111 This implicates that availability of amino acids is important for normal satellite cell function in COPD and that restoration of normal amino acid levels may be required for muscle maintenance. The gene discussed is MSTN; the disease is chronic obstructive pulmonary disease.