These findings suggest that two types of MAPK pathway inhibitors, targeting different nodes of the pathway (MEK, ERK), enhance the therapeutic efficacy of exarafenib in BRAF-mutant lung cancer cells by effectively disrupting both conventional oncogenic-BRAF signaling (predominant in parental cells and non-treated resistant cells) and ARAF-KSR1-mediated bypass signaling (activated in resistant cells under drug treatment). This evidence concerns the gene ARAF and lung carcinoma.