One study even proposed that TP73, p15, p16 and ARF methylation is an early event in MM pathogenesis because of hypermethylation in both MGUS and MM samples, while SOCS-1 methylation was present in higher abundance in MM samples compared to MGUS and thus may be involved in the progression of MGUS to MM [58]. This evidence concerns the gene CDKN2B and Miyoshi myopathy.