Lin28b has been implicated as a key regulator of both leukemia pathogenesis and lipid metabolism, raising the possibility that Lin28b induction may play a key role in regulating lipid metabolism in Rpl22−/− leukemias.68–75 We have previously shown that Rpl22 loss promotes development of T acute lymphoblastic leukemia (T-ALL) through Lin28b induction.22Lin28b is also one of the most upregulated genes in leukemias that arose in the MLL-AF9 Tg Rpl22−/− mice (Figures 7A–7E). The gene discussed is MLLT3; the disease is leukemia.