Of note, the recent discovery of acquired mutations in MEF2C in a subset of immature T-ALL patients together with the observation that MEF2C can bind to the LMO2 promoters has already established a precedent for LMO2 function as a potential leukaemia oncogene in this subset of ‘phenotypically early' T-ALL.17 Here, LMO2 is linked to acute lymphoblastic leukemia.