In line with this and other data demonstrating the absence of KIT D816V in myeloid blasts of 50% of SM-AML cases [20], we confirmed the absence of KIT D816V but the presence of additional somatic mutations in CD34+ cells in 5 of 6 SM-AML cases, indicating that the additional somatic mutations rather than KIT D816V are the driving force for progression to secondary AML. Here, KIT is linked to acute myeloid leukemia.