PRMT1‐mediated methylation of dual‐specificity phosphatase 4 triggers its ubiquitylation and degradation, leading to activation of p38 kinase and blockade of megakaryocyte differentiation.[35] Recent studies have demonstrated that PRMT1 is highly expressed in MM patients and promotes MM progression in vitro and in vivo, suggesting that PRMT1 may be a potential therapeutic vulnerability in MM. Here, PRMT1 is linked to Miyoshi myopathy.