Sato et al. designed gRNAs to target EZR intron 9 and ROS1 intron 33 and successfully generated EZR/ROS1 fusions in HBECp53 lung adenocarcinoma cells, which highly induced the phosphorylation of MEK and ERK, and the MEK/ERK signaling pathway can mediate the primary or acquired resistance to ROS11 TKIs in ROS1 rearranged lung adenocarcinoma patients. The gene discussed is ROS1; the disease is lung adenocarcinoma.