The TYRO3, AXL (also known as UFO) and MERTK (TAM) family of receptor tyrosine 
kinases (RTKs) are aberrantly expressed in multiple haematological and 
epithelial malignancies. Rather than functioning as oncogenic drivers, their 
induction in tumour cells predominately promotes survival, chemoresistance and 
motility. The unique mode of maximal activation of this RTK family requires an 
extracellular lipid–protein complex. For example, the protein ligand, growth 
arrest-specific protein 6 (GAS6), binds to phosphatidylserine (PtdSer) that is 
externalized on apoptotic cell membranes, which activates MERTK on macrophages. 
This triggers engulfment of apoptotic material and subsequent anti-inflammatory 
macrophage polarization. In tumours, autocrine and paracrine ligands and 
apoptotic cells are abundant, which provide a survival signal to the tumour cell 
and favour an anti-inflammatory, immunosuppressive microenvironment. Thus, TAM 
kinase inhibition could stimulate antitumour immunity, reduce tumour cell 
survival, enhance chemosensitivity and diminish metastatic potential.