AXL and neoplasm: The aberrant upregulation of the epidermal growth factor receptor (EGFR) and other receptor tyrosine kinases, such as the transforming growth factor beta receptor (TβR) and AXL, in NSCLC tumors is associated with poor outcomes; meanwhile, their overexpression activates the downstream PI3K/Akt/mTOR, Raf/MEK/ERK, and JAK/STAT pro-oncogenic signaling pathways, resulting in tumor proliferation, angiogenesis, migration and invasion, and anti-apoptosis [2,3,4].