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. This evidence concerns the gene AKT1 and neoplasm.