Moreover, the ability of Rpl22-deficient leukemias to form colonies was preferentially dependent upon the transcription factor PPARδ, a master regulator of FAO that has been implicated in the ability of FAO to promote HSC renewal (Figure 5F).47 Indeed, short hairpin RNA (shRNA) knockdown of Ppard selectively attenuated colony formation by Rpl22−/− leukemias (Figure 5F), indicating that Rpl22 loss promotes leukemic colony formation by upregulating FAO in a PPARδ-dependent manner. Here, RPL22 is linked to leukemia.