This is often accompanied by overexpression and activation of other receptor tyrosine kinases such as c-MET (also called hepatocyte growth factor receptor), HER2, fibroblast growth factor receptor (FGFR) and AXL and is also associated with resistance to EGFR-TKIs of tumors with EGFR activating mutations (e.g., in NSCLC) [131]. This evidence concerns the gene ERBB2 and non-small cell lung carcinoma.