Nonetheless, a large proportion of the lower abundance proteins plays a critical role in MM survival and proliferation, including cell cycle genes (such as cyclins, aurora kinases and CDC members [36]), kinases (e.g. PIM2 [49]), transcription factors (MYC [33, 34]) and TCF3, which might cooperate with MYC as an oncogenic axis [50]. This evidence concerns the gene MYC and Miyoshi myopathy.