Pathological B-cell receptor (BCR) signaling represents an important driver of malignant transformation in MCL, which is evident from the stereotyped, biased immunoglobulin heavy chain variable region gene (IGHV) repertoire in most MCL cases1, increased expression of BCR signaling components2,3, and strong, albeit short-lived, clinical responses to ibrutinib, which targets the BCR-downstream Bruton’s tyrosine kinase (BTK)4,5. This evidence concerns the gene BCR and mantle cell lymphoma.