We believe that MerTK and Axl are appropriate targets for therapy against glioblastoma because they exhibit little to no expression at both the mRNA and protein level in the normal human brain but are upregulated in glioblastoma and are readily activated by the ubiquitously present Gas6 which is available in the CNS in the normal and the diseased state [36]. Here, AXL is linked to glioblastoma.