Previous studies reported IGF-IR expression in 29–36% of TNBC (53) and in certain studies IGF-IR overexpression in TNBC was attributed to either mutations in tumor suppressor genes, including p53 and BRCA1, which repress the IGF-IR promoter (54), or to the amplification of IGF-IR in basal or HER-2 positive BC. The gene discussed is IGF1R; the disease is breast cancer.