In EGFR-mutant NSCLCs, up-regulated EGFR signaling increases VEGF through hypoxia-independent mechanisms, and elevated VEGF, in turn, contributes to the emergence of resistance to EGFR tyrosine kinase inhibitors (TKIs) [34], and EGFR, similar to VEGFR-2, can be expressed on tumor-associated endothelial cells [33]. Here, EGFR is linked to neoplasm.