This proportion of LMO1-positive T-ALL samples is similar to that previously reported where a significant subset of patients were found to express high levels of LMO1, often with no evidence of a chromosomal translocation involving the LMO1 locus.3 Moreover, LMO1 knockdown in Jurkat cells severely compromises their proliferative capacity (Figure 3d) pointing to a non-redundant role for LMO1 in leukaemia maintenance. The gene discussed is LMO1; the disease is acute lymphoblastic leukemia.