Additionally, the tumor suppressor OPCML was found to interact and promote AXL inactivation in cholesterol-rich, detergent insoluble membrane compartments, where proximity to another tumor suppressor, PTPRG phosphatase, resulted in AXL-dephosphorylation, preventing AXL-mediated transactivation of other RTKs (cMET and EGFR) and downstream signaling (51). Here, AXL is linked to neoplasm.