AKT1 and Miyoshi myopathy: In addition, CXCR4 expression is abnormally elevated in MM extramedullary infiltration and plasma cell tumors [138], and blocking the CXCL12/CXCR4 axis could reduce its interaction with IL-6, decrease adhesion-mediated chemoresistance in MM cells, and induce cell apoptosis; mechanistically, SDF-1/CXCR4 may up-regulate the expression of IL-6 through the activation of the P13K/AKT signaling pathway, thereby affecting the chemoresistance mediated by adhesion in MM cells [139].