Evidence that interruption of the MEK1/2/ERK1/2 pathway down-regulates Mcl-1 expression [32] and/or alters its associations with pro-apoptotic effectors (e.g., Bak and Bim) [33]–[35] raised the possibility the Chk1/MEK1/2 inhibitor strategy might be active in the face of Mcl-1-related forms of drug resistance in MM. This evidence concerns the gene BAK1 and Miyoshi myopathy.