On the contrary, certain spectrum of the mutations in AML have already been implicated to possibly arise from an underlying MDS clone, or after a leukemogenic therapy (t-AML), in particular, the presence of the splicing gene mutations (SRSF2, SF3B1, U2AF1, and ZRSR2), has been established to be more than 95% specific for the diagnosis of secondary AML (s-AML) [84]. Here, SF3B1 is linked to myelodysplastic syndrome.