 KMT2C and KMT2D are two important epigenetic genes that are often mutated in cancer. KMT2C has been identified as a tumor suppressor in acute myeloid leukemia, AML. However, the role of KMT2D in AML remains unclear. In this study, researchers investigated the effects of KMT2D on AML cells and found that KMT2D deficiency leads to the activation of the MTR pathway, which results in abnormal ribosome biogenesis and decreased survival of leachemic mice. This suggests that KMT2D is a tumor suppressor in AML and that targeting the MTR pathway could be a potential therapeutic strategy for treating AML patients. This article was authored by Jean Su, Aileen Zhong, Sean Zhang, and others.