Our results suggest that this occurs by the following sequence of events: (1) Ets2 is upregulated by CKD; (2) TLR13 levels are increased by the activation of ETS2; (3) TLR13 recruits IRF3 to increase its serine phosphorylation, thereby impairing intracellular AKT signaling; and (4) increased levels of TLR13 promote skeletal muscle atrophy. The gene discussed is AKT1; the disease is chronic kidney disease.