For example, PSMB5 mutations have been shown to reduce binding of bortezomib (Btz) and carfilzomib (Crflz) to the proteasome in MM and non-MM cell models of PI resistance [2–6], alterations in redox homeostasis have been implicated in protecting MM cells from PI-induced oxidative damage and cell death [6–8], and adaptations involving the cellular protein folding machinery and energy regulation have been implicated in the PI resistance phenotype [6, 9]. This evidence concerns the gene PSMB5 and Miyoshi myopathy.