The oncogenic contribution of TKF to tumor maintenance can nevertheless vary according to several variables, including: (i) the properties of each fusion; (ii) the cellular context and the tumor microenvironment; (iii) the disease stage and evolution phase [28, 49]; (iv) the degree of oncogenic addiction to the TKF (e.g. ROS1-positive NSCLCs show better response to Crizotinib than ALK-positive NSLCLs) [50]; (v) the presence of concomitant genomic aberrations [30, 51]. This evidence concerns the gene ALK and neoplasm.