For example, expression alteration of genes such as Cyclin D1, gp130, and MAF parallel the dysregulation of these genes identified in human MM cells, which are variously driven by recurrent chromosomal translocations, gene amplification, and/or transcriptional mechanisms and represent essential elements in the genesis and progression of human MM (Kuehl and Bergsagel, 2002). The gene discussed is MAF; the disease is Miyoshi myopathy.