Moreover, high ADAR1 expression and Alu-dependent GLI1 RNA editing were also maintained in vivo (Supplementary Fig. 3e–h). Furthermore, this primagraft model propagated MM in serially transplanted recipient mice that recapitulated the engraftment phenotype observed in primary MM9-transplanted mice, as assessed by clonal light chain production in serum, and human CD138+/CD319+/CD38high/CD45dim cell engraftment in BM, SP, L, and PC (Fig. 3e, f; Supplementary Fig. 3i). This evidence concerns the gene ADAR and Miyoshi myopathy.