“…HPC1 (1q24–q25), PCaP (1q42‐q43), HPCX (Xq27–q28), CAPB (1p36), HPC20 (20q13), HPC2/ECAC2 (17p11) and 10q25 [32–40], but confirmatory studies at these loci have produced discordant results. Although an autosomal dominant model has been shown to provide the best model of the familial aggregation of prostate cancer in many studies [41–46], some analyses suggest that multiple alleles, each conferring modest risks such as RNASEL variants [47], may be responsible for most inherited disease [48]. The involvement of low‐penetrance alleles whose effect may be modified by environmental effects, together with locus heterogeneity, provides an explanation for the difficulties with identifying a gene through linkage.…”