For example, recent results in mouse models suggested dose-dependent effects of SIRT1 expression levels on cancer development, i.e. intestine-specific heterozygous deletion of Sirt1 in mice resulted in enhanced tumour formation by enhancing glutamine metabolism, while homozygous deletion of Sirt1 in mice showed reduced cancer development by triggering cellular apoptotic pathways46. This evidence concerns the gene SIRT1 and cancer.