HINT1 and ovarian neoplasm: Preliminary evidence for HINT1’s function in tumorigenesis comes from homozygous or heterozygous deletion of HINT1 in mice, which caused a marked increase in susceptibility to chemical carcinogen-induced malignant tumors, such as gastric tumors, mammary tumors, and ovarian tumors, and increased the occurrence of several types of spontaneous tumors with aging4,5, indicating that HINT1 may have a role as a haploinsufficient tumor suppressor in several malignant cancer types.