However, we consider this possibility highly unlikely for the following reasons: (a) cultured 4T1 cells did not produce IGF2 and explanted tumor specimens contained only trace amounts of IGF2 mRNA; (b) IGF2 binds to IR-A with a 7–10 lower binding affinity respect to insulin, and, therefore, can displace insulin binding only when present at molar excess; (c) especially in insulin glargine-treated mice, the tumor IR-A is expected to be saturated by insulin that cannot be displaced by the lower affinity ligand, IGF2 [4]. The gene discussed is IGF2; the disease is neoplasm.