A study evaluating the activity of Wnt/β-catenin signaling by transfecting AML and normal progenitors with a TCF/LEF reporter construct, found that in the majority of the AML samples, the TCF/LEF pathway was constitutively active, which was supported by other studies showing overexpression of β-catenin both in AML cell lines and patient samples[101,103]. The gene discussed is HNF4A; the disease is acute myeloid leukemia.