ALK and neoplasm: Through sequencing on longitudinal tumor biopsies from lung cancer patients resistant to third-generation ALK inhibitor lorlatinib, combined with the in vivo studies on patient-derived cell lines, Recondo et al. not only found that epithelial-mesenchymal transition (EMT) might mediate lorlatinib resistance, but also identified three mutations in the ALK kinase domain featuring the drug resistance: ALK L1196M/D1203N, F1174L/G1202R, and C1156Y/G1269A (Recondo et al., 2020).