To this end, we used an established zebrafish model of T-ALL, where tumour development is driven by the expression of the mouse c-Myc gene under the control of the zebrafish rag2 promoter42 (Fig. 9c); this model was chosen, because the c-Myc gene is commonly upregulated in Notch1-dependent T-ALL14, which represents one of the major groups of human T-ALLs43. The gene discussed is NOTCH1; the disease is neoplasm.