Such a model then also focuses attention onto the molecular events that cause breakdown of the epigenetic processes that keep the LMO1 locus repressed in normal haematopoietic cells, a better understanding of which would not only provide new insights into the pathogenesis of T-ALL, but may also open up new treatment opportunities, especially in light of the major current investment into the development of small molecule drugs targeting the epigenetic machinery.44 Here, LMO1 is linked to acute lymphoblastic leukemia.