The first studies describing a role for Wnt in AML showed that AML fusion proteins, such as AML1-ETO, PML-RARα, and PLZF-RARα specifically activated γ-catenin (also known as plakoglobin), the homologue of β-catenin, and lead to enhanced plakoglobin-LEF complexes, hence higher active Wnt signaling [16,17]. The gene discussed is RUNX1T1; the disease is acute myeloid leukemia.