In MM cell lines, as well as in other cancer cell types, SFKs and RTKs, such as EGFR and MET, are often concomitantly activated and can positively regulate each other and promote cell survival and resistance to single tyrosine kinase inhibition, by redundantly signaling to the same downstream pathways, including PI3K-AKT-mTOR and MAPK [31]. This evidence concerns the gene MTOR and Miyoshi myopathy.