These acquired bypass mechanisms of resistance included MET amplification; activating mutations in NRAS, BRAF, MAP 2 K1, and RET; oncogenic fusions involving ALK, RET, BRAF, RAF1, and FGFR3; and loss-of-function mutations in NF1 and PTEN. Thirdly, histologic transformation from lung adenocarcinoma to squamous-cell carcinoma was observed without identification of any other resistance mechanisms. Here, BRAF is linked to lung adenocarcinoma.