The absence of STAT5A in hematopoietic progenitors does not reduce CML clonality. Genomic DNA was prepared from P210/STAT5A^–/– and P210/STAT5A^+/+ leukemia cells isolated from mice with the CML-like disease, digested with the restriction enzyme Bgl II, and analyzed by Southern blot to assess the clonality of proviral integration. The number of unique leukemic clones is shown at the top for each CML animal. Size markers are shown at far right. Note that the neomycin resistance gene probe also detects the neomycin resistance cassette present in the STAT5A targeting vector (arrow).