In cases of adult acute myeloid leukaemias (AML) driven by constitutive activation of the FMS-like tyrosine kinase 3 (FLT3) present in 30–35% of cases [122]; Leukaemias well characterised by redox dysfunction [25], increased activity of the NHEJ DSBs repair pathway is also seen and regulated by the phosphorylation of S2612 DNA-PK [123]. This evidence concerns the gene PRKDC and acute myeloid leukemia.