Increased expression of AMPD3 in skeletal muscle of patients with CHF may reflect a fuel shift toward increased catabolism of amino acids and thus provide a novel mechanism linking metabolic dysregulation and muscle wasting in patients with CHF given AMPD3 is upregulated in various atrophic conditions in animal models such as disuse, starvation, cancer, and denervation.14 The gene discussed is AMPD3; the disease is cancer.