Studies have shown that the affinity of Igfbp3 for IGF-I/II was lost when its residues I56, L80, and L81 were substituted by glycine (G), which prevented apoptosis and also promoted the tumor growth in vivo and in vitro (Buckway et al., 2001; Takaoka et al., 2007; Natsuizaka et al., 2012). The gene discussed is IGFBP3; the disease is neoplasm.