IGF‐1 plays a critical role in maintaining CSCs characteristics and facilitating tumor cell proliferation, invasion, and metastasis.[43, 44, 45] Previous studies have shown that IGF‐1 binds to its receptor IGF1R, initiating downstream activation of the Akt/mTOR pathway, thereby promoting tumor cell proliferation and inducing drug resistance.[26, 46] In this study, we found that IGF‐1 secreted by CAFs upregulated c‐Myc expression to enhance tumor stemness via the IGF1R/Akt/mTOR pathway. The gene discussed is MTOR; the disease is neoplasm.