Though the molecular mechanisms underlying acquired resistance to EGFR TKI and crizotinib in EGFR/ALK co-altered patients were similar to those in typical EGFR mutation and ALK rearrangement patients, such as EGFR exon 20 T790M mutation and pathologic transformation from adenocarcinoma to SCLC small-cell lung cancer have been linked to resistance to erlotinib. This evidence concerns the gene ALK and adenocarcinoma.