To test the hypothesis that IL-6 independency could occur through cell-autonomous compensatory mechanisms, we analyzed the Notch signaling pathway activity in the human myeloma cell lines (HMCLs) CMA-03 and CMA-03/06, a cell model of MM acquisition of IL-6 independency previously established by our group [51, 52]. The gene discussed is IL6; the disease is Miyoshi myopathy.