A role for antigen recognition by the BCR in selection of the tumor clone or driving persistence via the BCR has been investigated in diverse B-cell tumors: it is clear that signalling via the BCR is implicated, as recent data from genome sequencing highlights abnormalities in key downstream pathways such as CARD11 in DLBCL, and constitutive activation of the PI3K pathway in lymphoma, or that the BCR itself is selectively modified to promote tumor: niche interactions, as in follicular lymphoma to potentially bypass a requirement for antigen (Review, [14]). This evidence concerns the gene BCR and lymphoma.