The only other potential mediator of the increased ZAG expression in cachexia is interferon-γ (IFNγ), which has been shown to strongly upregulate expression in human epithelial cell lines (Brysk et al, 1997), and has been suggested to be responsible for the development of cachexia in the Lewis lung tumour model (Matthys et al, 1991b). This evidence concerns the gene IFNG and Cachexia.