In principle, there appear to be four potential ways of triggering an activated B cell receptor in the pathogenetic course towards mantle cell lymphoma development: (i) “classical antigenic drive” by antigen binding to the CDRs of the BCR, (ii) antigen-independent autologous signaling of the BCR, e.g., by aberrations within CD79, (iii) superantigen-triggered BCR activation, or (iv) a combination of (i) and (iii) with superantigens facilitating BCR activation by low level (may be due to low affinity) antigen binding or CD79 aberrations (Fig. 4). The gene discussed is BCR; the disease is mantle cell lymphoma.