Taken together, these results suggest that in this cancer cell model of acquired resistance to four different TKIs, activation of AKT- and MAPK-driven intracellular signals, which could be activated also by other cell membrane growth factor receptors such as IGF-1R and/or MET, may be responsible for cancer cell growth in the presence of either selective anti-EGFR TKIs, such as gefitinib or erlotinib, or in the presence of broad spectrum TKIs, such as vandetanib or sorafenib. This evidence concerns the gene MET and cancer.