In this context, the ability of the immunocompetent Vk*MYC mouse model to develop a plasma cell tumor with canonical and spontaneous APOBEC mutational activity both represents a confirmation of the genomic similarities between human and Vk*MYC mice MM, as well as a unique model system to explore how and why APOBEC activate during cancer development. The gene discussed is MYC; the disease is plasma cell neoplasm.