OPCML exerts its tumor suppressor effect by inhibiting several cancer hallmark phenotypes in vitro, and abrogating tumorigenesis in vivo, by downregulating/inactivating a specific spectrum of Receptor Tyrosine Kinases (RTKs), including EphA2, FGFR1, FGFR3, HER2, HER4, and AXL [16,17,18,19,20,21,22,23]. The gene discussed is AXL; the disease is neoplasm.