ALK-rearranged NSCLC tumors can lose their reliance on ALK, and instead become dependent on the alternative activation of signaling axes, for example, alterations in EGFR, KRAS/MAPK, cKIT, MET, HER2/HER3, AXL and IGF-1/IGF-1R pathways, among others [12,25,26]. This evidence concerns the gene ERBB2 and non-small cell lung carcinoma.