Taken together, we modeled the development of AML from antecedent CH and MPN in this patient, whereby TET2/JAK2 mutant preleukemic HSCs acquired additional mutations in TP53 and GATA2 genes, followed by LOH in a subfraction of LSCs, which had the clonogenic advantage to capitulate AML (Fig. 5I). The gene discussed is TP53; the disease is acute myeloid leukemia.