For example, in a transgenic mouse model of CHF with cardiac-specific overexpression of calsequestrin, slow-twitch, oxidative muscle maintained muscle mass, whereas fast-twitch, glycolytic muscles underwent profound atrophy with sarcomere degeneration, loss of mitochondria and dramatic induction of the muscle atrophy F-box (MAFbx)/Atrogin-1 mRNA in the proteasome degradation system [67]. The gene discussed is FBXO32; the disease is congestive heart failure.