Among these, the upregulation of cyclin-dependent kinase 6 (CDK6), the reduced expression of nuclear receptor co-repressors 2 (NCOR2), the upregulation of the MEK/ERK pathway by modulating the tumor necrosis factor receptor-associated factor 2 (TRAF2), or interleukin 6 (IL-6)-mediated activation of the JAK/STAT3 pathway were identified as major factors that may modulate sensitivity or resistance to len in MM in either in vitro or in vivo studies [14,26,27]. This evidence concerns the gene CDK6 and Miyoshi myopathy.