Indeed, tyrosine kinases such as EGFR, MET, and SFKs can redundantly signal to downstream oncogenic pathways, including PI3K-AKT-mTOR and MAPK (Figure 2); thus, inhibition of one of these tyrosine kinases alone in MM cells might be ineffective if the other kinases induce the same cell proliferation/survival pathways [31]. This evidence concerns the gene MET and Miyoshi myopathy.