Overall, MM plasma cell exhaustion, which characterizes patients who responded to VTD achieving CR, might be biologically accounted for by the deregulation of MM's key biology pathways, i.e. NFkB, (a), IL6R, VEGF and IGF1R signalling pathways; (b) basic cell processes (cell cycle and apoptosis regulation, cell homing and migration); (c) other signal transduction pathways related to initiation of RNA translation (i.e. eiF2, eiF4 and p70S6K signalling), to DNA damage control (p53 signalling) and to inflammatory response (CD40 signalling). This evidence concerns the gene TP53 and Miyoshi myopathy.