IGF-1R-antagonistic antibodies (αIR3) interfering with the IGF-1 autocrine loop or with the IGF-1 axis were later shown to have comparable effects in profoundly suppressing serum-induced survival and potentiate apoptosis induced by glucocorticoids and death receptors, i.e. Fas, in MM cells (52,53,21,54). This evidence concerns the gene IGF1R and Miyoshi myopathy.