Initiating lesions arise from the activity of the DNA activation-induced cytidine deaminase (AID) within the germinal center, while late mutations associated with progression to MM arise from the aberrant activity of the APOBEC (apolipoprotein B mRNA editing catalytic polypeptide-like) family of cytidine deaminases, a mutational process common to many cancers and absent in normal plasma cells (PCs) [17,21,22]. This evidence concerns the gene AICDA and Miyoshi myopathy.