Although this proportion is lower in comparison to the 80% we have previously reported for human MM and its progressive precursor conditions6, the significant discovery that Vk*MYC MM spontaneously develops APOBEC mutagenesis is a critical finding, considering that no other mouse model of MM has been reported to spontaneously acquire an APOBEC mutational signature (see Methods)30,31. Here, MYC is linked to Miyoshi myopathy.