In vivo, hyperinsulinemia may induce the action of EC in multiple malignant phenotypes through the activation of several important receptor-mediated pathways, such as insulin receptors and insulin-like growth factor 1 receptor (IGF-1R), and the typical signaling pathways involved in these receptors include the phosphatidylinositol 3-kinase (PI3K)/extracellular signal-regulated kinase (ERK/AKT) and mitogen-activated protein kinase (MAPK) pathways [21, 22]. The gene discussed is IGF1R; the disease is hyperinsulinism.