if the drug has two targets then one can't be sure in general which one (or even the combination) is the key to a particular response.
Many patients with advanced lung cancer carry at least one of the known driver mutations - KRAS, EGFR, HER2, BRAF, PIK3CA, AKT1, MEK1, NRAS, or oncogenic changes - ALK rearrangements and MET amplifications. But if you perform genetic testing on tumor biopsies at the time of diagnosis, you can have a pretty good idea if there's an 'oncogene addiction' of certain type that will most likely respond to a targeted therapy for some time (until resistance emerges).