These mutations cause altered expression of EGFR, which results in the activation of downstream signaling pathways, such as the MAPK, FAK/Paxillin, and PI3K/AKT/mTOR pathways, which, in turn, promotes tumor cell proliferation, survival, migration, and angiogenesis [48].According to flow cytometry results, we observed statistically significant increases in VEGFR-2 and NP-1 protein levels on the cell surfaces of EGFR-TKI-resistant cells compared to their corresponding TKI-sensitive cell lines (Figure 3). Here, MTOR is linked to neoplasm.