The administration of ghrelin as a treatment for cancer cachexia patients has been evaluated [59]. In vitro evidence showed that the expression of atrogenes through PI3Kβ-, mTORC2-, and p38-mediated pathways in myotubes and dexamethasone-induced muscle atrophy was inhibited by acylated and nonacylated ghrelin, suggesting that this peptide may be able to prevent muscular atrophy [12]. The gene discussed is GHRL; the disease is muscular atrophy.