Two distinct BcR IGs derived from CLL subset no. 2 cases promoted Ca2+ influx when transduced in TKO cells (Fig. 6), and this property could be abolished only by the specific mutations (Asp50LAla/Asp52LAla in the paratope, Lys16LAla, or Arg110LGly in the epitope) engineered to disrupt the contacts observed in the crystal structure (Fig. 6). This evidence concerns the gene BCR and B-cell chronic lymphocytic leukemia.