It should be noted that these tumours represent ‘models’ as the genetic backgrounds that we employed in this study to overcome cellular senescence induced by loss of TSC2 function are apparently not reflected in the genetics of human renal AMLs, for example, genetic mutations or deletions of TP53, CDKN2A or other senescence regulating tumour suppressor genes have not been observed in AML tumours. The gene discussed is CDKN2A; the disease is acute myeloid leukemia.