Previously, progression and characteristics of AML were linked to several key pathways (10, 11), including inactivation of tumor suppressors [such as TP53 and Wilm’s Tumor-1 (WT1)], gain-of-function mutation of oncogenic kinases (such as FLT3, NRAS, and KRAS), and stem cell transcription factors (TFs) [such as rearrangement and/or overexpression of HOX cluster genes and their cofactors such as MEIS1 (12–14)], as well as inactivating mutation of differentiation-promoting TFs (such as PU.1 and CEBP/α). Here, WT1 is linked to acute myeloid leukemia.