Taken together, these findings suggest that the heightened activation of YAP, as observed in EGFR- or KRAS-mutated lung adenocarcinoma, as well as BRAF-mutant lung cancer cells and KRAS-mutant NSCLC tumors, might play a significant role in conferring resistance to MEK inhibition. Here, YAP1 is linked to non-small cell lung carcinoma.