Our major findings are as follows: 1) The muscle signatures associated with the disease were strikingly similar in MG patients and in induced EAMG in rats, and revealed the involvement of IL-6 and IGF-1 pathways; 2) IL-6 had an altered expression in the muscles of EAMG models and MG muscle compared to controls, and was induced in cultured muscle cells treated with anti-AChR antibodies; 3) Akt, a downstream effector of IGF-1 pathway on which IL-6 is known to have a negative effect, exhibited defective phosphorylation in cultured muscle cells treated with anti-AChR antibodies. The gene discussed is IGF1; the disease is myasthenia gravis.