IGF1R and neoplasm: Also, Cheng et al. (2022), study reported that the binding of GPC3 to IGF-1R through its N-terminal proline-rich domain, induces the phosphorylation of IGF-1R, extracellular signal-regulated kinase (ERK) and c-Myc expression causing cell proliferation and tumor progression in addition to, activation of AKT pathway that leads to protein synthesis and growth [43].