After binding to a ligand, IGF1R is autophosphorylated, which activates its tyrosine kinase function, and it then interacts with adaptor molecules such as insulin receptor substrates and Shc, thus activating downstream protein kinases, including those in the PI3K/AKT and MAPK/ERK1/2 signaling pathways that regulate the growth and survival of cancer cells [46]. This evidence concerns the gene IGF1R and cancer.