A recent study has further highlighted the importance of CD79B mutations for surface expression of the BCR in ABC DLBCL cells and provided a rationale for the frequently observed co-occurrence of CD79B and MYD88 mutations in B-cell malignancies [40]: While CD79B mutations alone are not sufficient to enhance NF-κB-mediated B-cell proliferation and MYD88 mutations on their own decrease surface IgM/BCR expression reminiscent of anergic B cells, the combination of CD79B and MYD88 mutations cooperates in plasmablastic differentiation [81]. This evidence concerns the gene BCR and diffuse large B-cell lymphoma.