Since studies of large panels of T-ALL have failed to find equivalent recombination-mediated deletions in the human NOTCH1 gene [32], this represents a mouse-specific tumour susceptibility that may contribute to their increased vulnerability to radiation-induced T cell tumours; though, the finding of a NOTCH1 Type 2 activating deletion (not recombination mediated) in a T-ALL patient [40] demonstrates that the mechanism has prima facie relevance to human cancers. The gene discussed is NOTCH1; the disease is acute lymphoblastic leukemia.