Studies have confirmed that coexistence of TP53 affects the efficacy of EGFR, ALK, and ROS1 TKIs therapy as determined by relatively short mPFS.[7] Moreover, ROS1 and TP53 co-mutation also shorten the mPFS of the patients with lung cancer as reported.[5,8] Therefore, we speculated that the patient’s resistance to crizotinib may be related to the coexistence of TP53 mutations. This evidence concerns the gene ALK and lung carcinoma.