ALK and lung adenocarcinoma: IGF-1R pathway activation can mediate resistance in both EGFR-mutant and EML4-ALK positive lung cancer.35–37 Overexpression of the tyrosine kinase AXL, which is able to engage multiple downstream signaling nodes also activated by EGFR, was identified by our group and others as a driver of EGFR inhibitor resistance.38 Similar findings were observed in ALK gene rearrangement positive lung adenocarcinoma.39