Even though there is agreement about loss/mutation of TP53 having negative impact on MM prognosis, MDR in 17p13.1 area in our dataset also included spermine N1-acetyltransferase SAT2, which has been reported to be significantly underexpressed in del(17p); it interacts with p65 subunit of the NF-κB pathway and thus is another possible candidate gene in this area [28]. This evidence concerns the gene TP53 and Miyoshi myopathy.