Recently, a research has indicated that EGFR-mutant NSCLC cells display a HIF-1α and VEGF-dependent phenotype and that in EGFR-mutant NSCLC cells, EGFR, but not hypoxia, regulates HIF-1a transcription and protein stability, whereas in EGFR WT NSCLC, hypoxia is the primary regulator of HIF-1α. This evidence concerns the gene EGFR and non-small cell lung carcinoma.