Since self-renewal and regulation of cell fate in LSCs is crucial for the development of the disease, we next studied LTβR signaling in a murine CML model45 CML-like disease was induced by injection of BCR-ABL1-GFP-transduced BL/6 or Ltbr−/− LSKs into nonirradiated BL/6 recipients (Fig. 6a). The gene discussed is LTBR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.