For example, PML NB–dependent activation of peroxisome proliferator-activated receptor (PPAR)γ co-activator-1α (PGC-1α), PPAR signaling and fatty acid β-oxidation were shown to provide a growth advantage to breast cancer cells (Carracedo et al, 2012), and controlled asymmetric division and maintenance of hematopoietic stem cells (Ito et al, 2012). This evidence concerns the gene PPARGC1A and breast carcinoma.