Notably however, both Tyro3 and Mertk become hyperactivated in the presence of phosphatidylserine (PS)-positive liposomes and apoptotic cells, implying that Mertk and Tyro3 may act as “PS sensors” for externalized PS on apoptotic cells and in the tumor microenvironment (13, 14). The gene discussed is TYRO3; the disease is neoplasm.