To test this hypothesis, we introduced the vnn1 gene deletion in p16Ink4A/p19Arf-deficient mice (p16/19−/−) which spontaneously develop various tumor types, including lymphomas, sarcomas, and carcinomas (Sharpless et al, 2002) and probed whether Vnn1 deficiency impacted the development of specific cancers and modulated their metabolic environment. Here, VNN1 is linked to carcinoma.