Studies in Ewing’s sarcoma cells treated with figitumumab, an IGF-IR antagonist, revealed that this antibody functioned as an IGF-1R-biased agonist through β-arrestin1 recruitment to the receptor, enhancing IGF-IR ubiquination and provoking Erk phosphorylation in the absence of Akt activation (92). This evidence concerns the gene IGF1R and Ewing sarcoma.