Prostatic carcinogenesis is a multistep process with well-documented stages. Although prostate cancer is a major cause of mortality many small tumor foci never progress to form clinically significant disease, indicating that the disease process may be regulated at more than one level. Carcinogenesis is accompanied by increasing genetic damage to prostatic epithelial cells, however the pattern of genetic lesions is inconsistent. The differentiation of stromal cells surrounding tumors is more fibroblastic and less muscular than in normal prostate. The present communication reviews the roles of both genetic and, stromally derived, epigenetic effects on prostatic tumorigenesis.