The redundancy of Notch ligands and the efficacy of Jagged1 and Jagged2 inhibition in reducing the excessive Notch signaling in MM cells, may provide the rational for an effective and safer Notch-directed approach to target MM patients bone disease and the associated co-morbidities, including increase in tumor burden [10], angiogenesis [12], drug resistance [35, 36] and inhibition of immune response [3, 11]. The gene discussed is JAG2; the disease is Miyoshi myopathy.