Overcoming these deficiencies may require introduction of the hallmark WM MYD88L265P point mutation24 to the BCL2+IL6+AID− model, which may be accomplished by crossing in a newly developed conditional transgene harboring this mutation.25 A complementary approach may be lentiviral gene transduction of BCL2+IL6+AID− B-cells with CXCR4WHIM mutant alleles26, 27 followed by adoptive transfer (AdT) of the modified B cells to a suitable host in which lymphoma formation takes place—as recently shown for AdT models of human myeloma.28, 29, 30. This evidence concerns the gene BCL2 and plasma cell myeloma.