Although it is still unclear whether KRAS mutations are actually associated with resistance to EGFR inhibitors in lung cancer,[22] aberrations of HGF signal are apparently involved in resistance to anti-EGFR and anti-VEGF targeted therapies.[23] Contrarily, FLT-3 and mTOR might represent potentially actionable targets, as the former is sensitive to drugs such as dovitinib, while the latter is sensitive to everolimus.[24]. This evidence concerns the gene FLT3 and lung cancer.