Owing to the distinct sets of RTKs activated in different KRAS-mutant NSCLC cells following MEK inhibitor-trametinib treatment, the heterogeneity of this adaptive resistance makes the use of combination therapies with a MEK inhibitor and a single-target RTK inhibitor impractical.26 To address this issue, we screened a pan-RTK inhibitor, anlotinib, which has demonstrated antitumor activity via the inhibition of VEGFR1, VEGFR2, VEGFR3, c-KIT, PDGFRα, FGFR1, FGFR2, and FGFR3,30–33,43–45 to block the adaptive resistance of the MEK inhibitor trametinib. This evidence concerns the gene KRAS and non-small cell lung carcinoma.