BRAF and lung adenocarcinoma: Studying BRAFV600E mutant lung adenocarcinoma, our group identified that a switch from expression of a full-length BRAFV600E to a shorter splice variant was capable of mediating resistance to the BRAF inhibitor vemurafenib.21 This splice variant is able to dimerize and activate downstream MAPK pathway signaling despite presence of the RAF inhibitor.