Prost et al. showed that PPARγ agonist, pioglitazone, can purge the residual CML LSC pool by downregulating expression of STAT5 and its downstream targets, Hif2a and Cited2, which are key regulators of the stemness of CML LSCs [25]. The gene discussed is PPARG; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.