To investigate the presence of cooperating mutations involved in the pathogenesis of Zeb2-induced leukaemias, and to determine to what extent this leukaemic mouse model recapitulates human T-ALL, we performed mutation analysis and array Comparative Genomic Hybridization profiling in control (P53/R26+/+) and Zeb2-overexpressing tumours (R26-Zeb2tg/tg and P53/R26-Zeb2tg/+ or P53/R26-Zeb2tg/tg). The gene discussed is TP53; the disease is neoplasm.