And activation of the IGF-1 and insulin receptors results in intracellular signaling cascades in both the extracellular signal-related kinase (ERK) and phosphatidylinositol-3 kinase (PI3K) pathways, producing downstream mitogenic, antiapoptotic, and proangiogenic effects that may favor tumor growth in EAC.[40] What is more, the study demonstrated that serum total and free IGF-1 levels are significantly increased among viscerally obese patients compared with normal weight controls, and among patients with EAC compared with Barrett esophagus (BE) and healthy controls.[41]. This evidence concerns the gene INSR and esophageal adenocarcinoma.