While MAF/MAFB translocated MM patients are characterized by a high APOBEC mutational contribution (i.e., hyper-APOBEC), mostly driven by APOBEC3A isoform, 80% of MM and progressive MM precursor conditions have a lower APOBEC mutational activity where the isoforms 3A and 3B play an equal role (i.e., canonical APOBEC)13,43,44. This evidence concerns the gene APOBEC3A and Miyoshi myopathy.