BCR response is highly correlated with TCL1 levels in the CLL cells and with the formation of activation complexes at the BCR, by TCL1, AKT and ZAP70 kinases.64 Interplay between TCL1 and BCR activity was also suggested by studies on dnRag1/TCL1 double-tg.65 Enforced BCR auto-reactivity, due to RAG1 impairment, induces an indolent accumulation of CD5+ B cells, similar to monoclonal B-cell lymphocytosis; the TCL1 overexpression provides an additional lesion on this background, promoting progression to CLL. The gene discussed is BCR; the disease is B-cell chronic lymphocytic leukemia.