AKT1 and Miyoshi myopathy: The possible mechanisms of drug resistance include MDR gene polymorphism and p-glycoprotein overexpression in MM cells, microenvironmental changes (cell adhesion, activation of cytokine-related antiapoptosis pathways such as the JAK/STAT and PI3K/AKT pathways), clonal evolution such as hyperexpression of the proteasome-related gene, PSMD4, related to chromosome 1q21 amplification, t(4;14) unbalanced translocation, and selected CD34+CD138+B7-H1+CD19− plasma cell accumulation after treatment.