Increased interactions between adhesion molecules of ECM (e.g., fibronectin, E-cadherin, or laminin) and integrins, heparin sulfate proteoglycans, or surface signal receptors on tumor cells results trigger anti-apoptotic properties of MM cells, leading to cell-adhesion–mediated drug resistance (CAM-DR) [18, 19]. This evidence concerns the gene CDH1 and Miyoshi myopathy.