Consequently, decreased AKT activation could permitdephosphorylation of FoXOs and thus translocation of FoXOs to the nucleus, where they areactivated and promote upregulation of genes related to protein degradation (53,66,68,69), namely atrogin-1 andubiquitin-conjugating enzyme E3, thus leading to cachexia. The gene discussed is FBXO32; the disease is Cachexia.