Characteristic landmarks of a fragile region, such as aphidicolin-induced hybrid breaks, HPV16 integration sites, pSV2neo integration sites, and deletion end points in cancer cell lines, have been identified within introns of FHIT[14]; however, these landmarks do not overlap with the region within intron 5 that we implicated in prostate cancer risk. The gene discussed is FHIT; the disease is prostate carcinoma.