LUAD can also adapt to the pressure of TKIs by activating bypass signaling pathways, which allow cancer cells to continue to grow despite the targeting of the driver gene mutations, like PI3K/AKT or RAF/MEK/ERK pathways [3,110], or by triggered mutations activating downstream effector molecules of the targeted cascade, like MAPK activation in both EGFR- and ALK-mutant NSCLC [111,112]. This evidence concerns the gene EGFR and non-small cell lung carcinoma.