Along with this, KDR amplification has been previously shown in non-small cell lung carcinoma to be associated with VEGF-induced elevated expression of KDR, p38, and mTOR pathway components, promoting a more invasive phenotype.41 Specifically, it was noted that there was phosphorylation of p38, elevated levels of HIF1α, and increased c-Met activation, correlating with increased angiogenesis and tumorigenesis. Here, HIF1A is linked to non-small cell lung carcinoma.