Combination therapies targeting more than one checkpoint in the cell proliferation pathway, such as blocking both the PI3K/mTOR and MEK pathways in the allografts of NF1/BRAF-mutated melanomas and dual EGFR, MEK inhibition concurrently in TKI-resistant NF1-deficient lung adenocarcinomas, may be superior to monotherapy [106, 110]. This evidence concerns the gene NF1 and lung adenocarcinoma.