A genetic component in prostate cancer has been recognized for decades. Through numerous epidemiological and molecular biological studies much evidence has accumulated in favor of a significant but heterogeneous hereditary component in prostate cancer (PCa) susceptibility. At first, segregation analyses supported the view that a number of high-risk loci contributed to the observed Mendelian inheritance of PCa. Consequent mapping efforts yielded several susceptibility loci across the genome. At three of these loci genes have been cloned and mutations identified. Their role in hereditary and sporadic disease, however, is still under debate and probably very modest. The current evidence supports the hypothesis that excess familial risk of PCa is due to the inheritance of multiple moderate-risk genetic variants. Although research on hereditary prostate cancer has improved our knowledge of the genetic etiology of the disease, a lot of questions still remain unanswered. Here, we aim to review the genetic epidemiological research and the mapping efforts in the field of hereditary PCa and the consequent problems that are encountered.