MTOR and neoplasm: For instance, PZR has been shown to accelerate CRC cell invasion and migration by enhancing FAK phosphorylation.[29] Additionally, HIF-2α has been implicated in activating CSCs in breast cancer through the PI3K/AKT/mTOR pathway.[30] Increasing evidence also suggests that ECM proteins create a biochemical and physical niche for CSCs, further promoting tumor progression.[31] Together, these findings emphasize the impact of specific genes on the “stemness” phenotype of cancer, providing valuable insights for developing targeted therapies to effectively eliminate CSCs.