For example, in patients with t(14;16) and t(14;20) translocations where MAF genes are overexpressed, it was shown that blocking MEK pathway could downregulate MAF, inhibit cell proliferation and sensitize MM cells to the drugs, indicating that MAF exploits a common pathway in both translocations and MEK would be an additional drug target for above patients [42, 43]. Here, MAF is linked to Miyoshi myopathy.