Therefore, while it would be possible that CO2-induced AMPK activation modulates autophagy via an alternative route including Serine 317 and Ser 777 phosphorylation of Ulk1 [92], it is also conceivable that a context-specific process limits the effects of CO2 on autophagy via AMPK, which could be defined if an animal model of CO2-retaining COPD-induced muscle wasting became available (see below). The gene discussed is PRKAA1; the disease is chronic obstructive pulmonary disease.