Almost every form of cancer in humans has been reported to aggregate in families. These familial clusters can be due to inheritance of a mutated cancer-susceptibility gene, though other explanations include chance association and shared exposures to environmental carcinogens. In recent years, the chromosomal locations of some cancer-predisposing genes have been mapped by the new techniques of molecular genetics. A few have been identified, including the hereditary retinoblastoma (Rb) gene, WT1 gene for Wilms’ tumor, neurofibromatosis type 1 gene, the APC gene of familial polyposis coli, and the p53 gene in Li-Fraumeni syndrome. The work of the Human Genome Project will soon lead to the identification of many more genes for hereditary diseases, including cancer. The proper use of genetic data on populations and individuals is a matter of growing concern. Some issues, such as autonomy, confidentiality, and nondiscrimination, are generic to testing for any heritable disease. These broader questions have been the subject of scholarly treatises, position papers, and legislation. Other issues are disease specific and determined by age at onset, disease severity, availability of treatment, mendelian inheritance pattern, and gene penetrance and expressivity. To date, discussions on testing for inherited mutations in cancer-susceptibility genes have been limited, perhaps because the cancers due to these mutations are rare (retinoblastoma and Wilms’ tumor) or are preceded by distinctive clinical manifestations (neurofibromatosis and familial adenomatous polyposis).