Using a mouse model based on retroviral transduction of BCR-ABL1 into bone marrow HSCs (Lin−Sca-1+c-Kit+CD150+) with conditional deletion of the Klf4 gene and subsequent transplantation of these cells into cytoablated recipient mice, we found that loss of KLF4 led to spontaneous regression of CML-like disease associated with progressive attrition of LSCs in the bone marrow and spleen14. The gene discussed is KLF4; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.