The 17p chromosomal region harbors the gene locus of TP53, an important tumor suppressor gene.[21] Deletion of this region is a recurrent cytogenetic abnormality present in 10–34% of MM cases along with disease progression and is considered an independent factor responsible for less favorable clinical outcome in MM patients.[2a,4b] In keeping with this notion, the lesions associated with short OS in multivariate analysis are +1q and del17p13 in MM,[21, 22] suggesting that the combined cytogenetic abnormality contributes to the progression of MM. This evidence concerns the gene TP53 and Miyoshi myopathy.