Genes related to the DNA repair pathway (including TP53, ATM, and ATR), G1/S cell cycle transition (including CCND1 and RB1), and epigenetic regulation (including HIST1H1E, KMT2C, and KDM6A) have also been reported to be recurrently mutated in MM cases, confirming their importance in the pathogenesis of MM [1,2,3,4]. The gene discussed is KMT2C; the disease is Miyoshi myopathy.