Though this study utilized MLL::AF9- rather MLL::ENL-driven AML as a model for fully transformed AML and LIN28B expression levels were higher in the transgenic models than occurs physiologically (Supplementary Fig. 1), the results are nevertheless consistent with our prior work showing that LIN28B impedes MLL::ENL-driven AML initiation by stabilizing MYBBP1A expression [11]. The gene discussed is MLLT3; the disease is acute myeloid leukemia.