In the advanced MM, the characteristics of DMKN-repressed EMT were associated with the disruption of MET/EMT cortical actin, greater expression of epithelial markers (E-cadherin and ZO-1), and lower expression of mesenchymal markers (N-cadherin, vimentin, and Snail) (Fig 6A). The gene discussed is DMKN; the disease is Miyoshi myopathy.