Therefore, we investigated whether MyD88-deficiency would influence leukemia development in our IgH.TEμ CLL mouse model, in which we previously showed that (i) CLL development is critically dependent on Btk and is accelerated in the presence of the CD19-hBtk transgene, and that (ii) malignant CLL B cells harbor high phosphorylation of Btk, Akt, and S6 (34, 36). The gene discussed is CD19; the disease is B-cell chronic lymphocytic leukemia.