Previous studies have shown that increased IGF1R expression activates pathways such as PI3K/AKT (Quail et al., 2016; Nemati et al., 2022), MAPK (Benito-Jardón et al., 2019), and Wnt (Zhang et al., 2015), thereby promoting proliferation and inhibiting apoptosis, exacerbating tumor malignancy. Here, IGF1R is linked to neoplasm.