Taken together, these data suggest that acceleration of CML in mice transplanted with MIG-BCR-ABL Gadd45b-/- progenitors compared to mice transplanted with wild type MIG-BCR-ABL progenitors is due to enhanced proliferation and decreased apoptosis of CML progenitors. The gene discussed is GADD45B; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.