Contrastingly, KDM6A remained unaltered in T-ALL cells and was found to play a tumour suppressor role as suggested by the identification of somatic loss-of-function mutations in paediatric and adult T-ALL patients as well as the finding that KDM6A deficiency hastened T-ALL progression in a NOTCH1-overexpressing murine model of T-ALL [28, 29]. The gene discussed is NOTCH1; the disease is acute lymphoblastic leukemia.