Use of gene-specific molecular probes has identified loss of the cyclin-dependent kinase-4 inhibitor (CDKN2A) (Prins, 1998; Illei, 2003), neurofibromatosis type 2 (NF2) (Bianchi, 1995; Sekido, 1995), p15 and p16 (Xio, 1995), p53 (Cote, 1991), and Fhit (Pylkkanen, 2004) genes in MM, supporting the role of cell cycle deregulation and inactivation of tumor suppressor genes in its pathogenesis. Here, CDKN2A is linked to Miyoshi myopathy.