Since preleukaemic erythroblastic cells expressing high levels of SPI1 exhibit replicative stress [32, 33], a deficiency in DNA repair and/or replicative stress responding proteins could increase the genetic instability and/or tumorigenic progression of SPI1-overexpressing preleukaemic blasts, revealing gene products and pathways involved in allowing leukaemia-initiated cells to progress. The gene discussed is SPI1; the disease is leukemia.