For example, hyperactive ERK and persistent mTOR signaling promote vemurafenib resistance in papillary thyroid cancer cells [46]; mTOR was associated with drug resistance in lung adenocarcinoma after radiation combined with TKI, and mTOR inhibition reverses drug resistance in lung adenocarcinoma after combined radiation and TKI therapy [47]; dual inhibition of AKT signaling/FLT3-ITD by the well-established orally available AKT inhibitor, A674563, overcomes FLT3 ligand-induced drug resistance in FLT3-ITD positive AML [48]. This evidence concerns the gene AKT1 and lung adenocarcinoma.