Current models posit that childhood BCP-ALL development often begins before birth, when for unknown reasons, an initial genetic event gives rise to a preleukemic clone (such as ETV6-RUNX1).15,16 The prevalence of preleukemia in neonates is still debated,28,29 but most likely, BCP-ALL develops in only a small proportion of children born with preleukemia.15 It has long been speculated that in these children, the malignant transformation of a preleukemic clone into ALL is triggered by a dysregulated immune response to infections.15,16. This evidence concerns the gene RUNX1 and myelodysplastic syndrome.