Although uPAR overexpression in human MM cell lines compared with MeT-5A and primary mesothelial cells has been previously reported [19, 35], we for the first time showed the association between uPAR overexpression and downstream PI3K/AKT/mTOR signaling with uPAR modulation in MM cells and xenograft tumors, as well as in human MM tissue samples. The gene discussed is AKT1; the disease is Miyoshi myopathy.