Conclusively, IMs are recruited to the lung metastatic site in a HIF-1α- or glycolysis-dependent manner, which is driven by Mint3, to release vascular endothelial growth factor (VEGF), and this secretion of VEGF induces the expression of E-selectin in the epithelial cells in the lung, which enables the extravasation of cancer cells [72]. The gene discussed is HIF1A; the disease is cancer.