IL6ST and Miyoshi myopathy: On the other hand, silencing c-myc or treatment of the cells with a c-myc inhibitor, 10058-F4, leads to a notable decrease of the mdig protein and all regulators on IL-6 pathway mentioned above, except pAkt (Fig. 7B,C), indicating that c-myc is an essential transcription factor in MM cells while mdig specifically cooperates with c-myc in promoting overexpression of GP130 and, consequently, causes amplification of the IL-6 signaling for cell survival and growth.