Taken together, these data suggested the relative higher level of phospho-EGFR was the mechanism of resistance to crizotinib; the EGFR exon 20 T790M mutations, pathology transformation from adenocarcinoma to SCLC and the relative higher level of phospho-ALK as molecular mechanisms of resistance to EGFR TKIs. The gene discussed is ALK; the disease is adenocarcinoma.