Here, we show that TET2 loss-of-function in CEBPADM AML leads to an aggressive disease phenotype by rebalancing the increased and suboptimal levels of GATA2 that are induced by hypermorphic CEBPANT mutations driving CEBPA-p30 isoform expression (see model in Fig. 7a). Here, CEBPA is linked to acute myeloid leukemia.