Since DNMT3B depletion strongly reduced c-MYC levels, a key oncogene overexpressed in about 70% of MM patients and linked with progression and adverse outcomes [36–38], and affected the expression levels of MYC targets, we next evaluated if DNMT3B targeting could be of benefit to patients with deregulated MYC. The gene discussed is DNMT3B; the disease is Miyoshi myopathy.