Similarly, resistance to Raf inhibition can result from upregulated levels of EGF, which activates EGFR, and drives downstream pathway activation in BRAFV600E mutant lung adenocarcinoma.21 Combinatorial inhibition of multiple kinases could be a therapeutic possibility in cases where activation of alternative receptor tyrosine kinases is responsible for driving resistance. The gene discussed is EGFR; the disease is lung adenocarcinoma.