Interestingly, the increase in the COPD myotube diameter after ascorbic acid treatment was correlated with the decreased expression of the atrophic marker MurF1, while the FoxO1 and MuRF1 expression decreases were positively correlated, suggesting that the ubiquitin/proteasome system is indeed involved in the oxidative stress-induced atrophy of COPD myotubes in vitro. The gene discussed is TRIM63; the disease is chronic obstructive pulmonary disease.