Furthermore, reactivation of KLF4 expression through modulation of PPARγ signaling, exerted a multifaceted tumor-suppressive effect in CDX2 positive myeloid leukemia cell lines and primary AML blasts (Faber et al., 2013), suggesting PPARγ agonists as a therapeutic modality in a large proportion of AML patients. The gene discussed is KLF4; the disease is acute myeloid leukemia.