Despite its lack of intrinsic kinase properties, IRS-1 is thought to be involved in tumorigenesis, it interacts with β-catenin, an important regulator of stem/progenitor cell fate, and levels of β-catenin target genes, such as c-myc and cyclin D1, are increased in mammary tumors that overexpress IRS-1 [61]. Here, MYC is linked to breast cancer.