It is notable that our findings provide the clear clinical, in vitro and invivo evidence for a solely oncogenic role of DOT1L regardless of MLL fusionpartners, in malignant transformation, invasion and metastasis of solid tumour.Numerous studies have proposed DOT1L as a crucial oncogene and potential therapeutictarget in human leukaemia, while only two studies have reported a role for DOT1L inaccelerating cell proliferation in some solid tumours, and prostate and lungcancers4, 34. The gene discussed is KMT2A; the disease is leukemia.