We propose a model according to which ERBB1 signals transmitted by activated ERBB1×ERBB1 homodimers or ERBB1×ERBB2 heterodimers contribute to the demonstrated adverse prognostic effects of ERBB1 [25] and ERBB2/HER2 (present study) in MM (Figure 6). This evidence concerns the gene ERBB2 and Miyoshi myopathy.