In acute lymphoblastic leukaemia (ALL), this effect is achieved through the activation of caspase 3 and the downregulation of oxidative stress [84], while in acute myeloid leukaemia (AML), the efficacy of this combined treatment is related to the inhibition of the FLT3 protein, a leukaemia-related protein marker overexpressed on the cell surface of leukaemic cells [85]. The gene discussed is CASP3; the disease is acute myeloid leukemia.