Both genetic abnormalities shortened the time to MM development in BIcγ1 and MIcγ1 mice, inducing a BM disease composed of GFP+CD138+B220−sIgM− PCs that secreted IgG or IgA, and was classified as MM (Fig. 1h,i and Extended Data Fig. 2a,b). This evidence concerns the gene CD79A and Miyoshi myopathy.