This was done by examining the signaling capacities of 13 CLL-derived BCRs that retained the IGHV-D-J and IGLV-J structures found on the original CLL B cell but expressed either IgM or IgD constant regions (Supplemental Table 3) using triple-knockout (TKO) cells that lack endogenous BCR expression but express 4-hydroxy-tamoxifen–inducible (4-OHT–inducible) ERT2-SLP-65 that enables Ca++ influx upon BCR signaling (42). This evidence concerns the gene MAPK3 and B-cell chronic lymphocytic leukemia.