Several mechanisms may operate in linking elevated insulin to endometrial cancer development, including growth-enhancing properties of insulin, increased levels of IGF-I receptors in the cancer tissue (Talavera et al, 1990; Roy et al, 1999) and suppressed gene expression of endometrial IGFBP-1, leading to increased biological activity of IGF-I (Irwin et al, 1993; Ayabe et al, 1997). This evidence concerns the gene IGF1R and cancer.