The disruption of muscle protein turnover with cancer cachexia corresponds to the chronic activation of adenosine monophosphate protein kinase (AMPK), which has been widely observed in preclinical cachexia models (Liu et al., 2019; Puppa et al., 2014; Segatto et al., 2017; White, Puppa, Gao, et al., 2013) and observed in human cachectic patients (Segatto et al., 2017). The gene discussed is PRKAA1; the disease is Cachexia.