BRAF and lung adenocarcinoma: In both A549 (KRAS-mut/BRAF-wt lung adenocarcinoma) and MiaPaCa2 (KRAS-mut/BRAF-wt PDAC) exposure to the BRAF-selective inhibitor dabrafenib for 4 h resulted in the dose-dependent phosphorylation of MEK, ERK and p90RSK, revealing a paradoxical MAPK activation (Fig. 1a); such paradoxical activation was maintained or increased up to 72 h (data not shown).