In a later study, Antony and co-authors were able to demonstrate that the tumor suppressor opioid-binding protein/cell adhesion molecule (OPCML), which is silenced in over 83% of ovarian carcinomas by loss of heterozygosity or by epigenetic mechanisms, is spatially restricted to the cholesterol-rich lipid rafts together with AXL, and when present, represses AXL-dependent oncogenic signaling through protein tyrosine phosphatase receptor type G (PTPRG) in a coordinated manner[162]. The gene discussed is AXL; the disease is ovarian carcinoma.