ALK rearrangements, primarily involving EML4-ALK fusions but also including KIF5B-ALK, TFG-ALK, and KLC1-ALK among others, are detected in approximately 3–5% of NSCLC cases.46 These cases share clinical features with EGFR mutations, such as adenocarcinoma histology and a history of mild or no smoking.47 Fusion transcripts containing the ALK kinase domain may promote kinase activation in downstream survival signaling, thereby providing vulnerability to TKI treatment.48 Here, ALK is linked to adenocarcinoma.