After eliminating known and targetable oncogenic genetic alterations (e.g., EGFR mutation(s), ALK rearrangement, ROS1 rearrangement, c-Met mutation(s), and c-Met amplification, Table S1) by tumors genetic testing and confirming no ALK rearrangement/fusion by ALK (D5F3) VENTANA immunohistochemical test (Supplementary Fig. 5, b and Supplementary Table 1), lung adenocarcinoma patients having failed first-line therapy with RDAA-positive and PD-L1 < 20% were enrolled and started the ALK inhibition treatment. The gene discussed is ALK; the disease is lung adenocarcinoma.