Our findings demonstrate poorer survival outcomes of patients with ROS1-rearranged NSCLC who harbored concomitant mutations in TP53, other tumor suppressor genes such as PTEN and RB1, and other oncogenic drivers such as EGFR, MET amplification, and KRAS. Our findings were consistent with the subgroup analysis of EUCROSS study on the shorter PFS of patients with ROS1-rearranged lung cancers with concomitant TP53 mutations, treated with crizotinib than their wild-type counterpart [31]. Here, KRAS is linked to non-small cell lung carcinoma.