Therefore, we conclude that under hypoxia, glioblastoma cells highly express HIF1α and HIF2α, which synergistically promote IGF1R expression, leading to the activation of downstream PI3K/AKT signaling through phosphorylation, thereby promoting cell proliferation and inhibiting apoptosis, exacerbating tumor malignancy (Figure 5D). The gene discussed is IGF1R; the disease is neoplasm.