Because both the Mo7e-p210 cell line and also cells from CML patients may have accumulated secondary mutations that could account for their defective capacity to form FANCD2 foci, in subsequent experiments healthy hematopoietic progenitors consisting in CB CD34+ cells transduced with vectors expressing the BCR/ABL oncogene were used. This evidence concerns the gene FANCD2 and chronic myelogenous leukemia, BCR-ABL1 positive.