While our focus here was on coincident overexpression or amplification of GAS6, AXL and MERTK as proxies of putative driver roles and relevant cabozantinib targets, our findings also suggest that a more comprehensive characterization of these pathways as drivers in tumor and immune compartments should inform efforts to optimally combine TKIs and checkpoint inhibitors for BCa treatment. The gene discussed is AXL; the disease is neoplasm.