Unlike the well-established roles of PML and PML-NBs in solid tumors and leukemia pathogenesis [which are effected through modulation of the activity of p53 (Bernardi et al., 2004), Atk (Trotman et al., 2006), mTOR, HIF1α (Bernardi et al., 2006), or mitochondrial regulatory pathways (Giorgi et al., 2010)], little is known about the role of this tumor suppressor in stem cell biology or the mechanisms of its regulation of cancer metabolism. The gene discussed is PML; the disease is neoplasm.