Genome wide association studies account for ~30% of heritable prostate cancers. This suggests that the majority of heritable prostate cancer risk lie in other single nucleotide polymorphisms (SNPs), or other genetic variations such as STRs. The lesser studied STR regions of the genome are increasingly recognised as important in (patho)-physiology. Thus, we assessed the potential of STRs to account for some of the missing heritability of prostate cancer by analysing data generated from ChIPseq and RNAseq to identify potentially functional STRs. Here we show recruitment of the androgen receptor and RNA Pol II, and histone modifications to specific STR sequences. Importantly, we show that some of these STRs are located within 200 bp of SNPs that we have recently found to confer prostate cancer risk, or that differentiate between men with different gleason grade tumours using the custom Illumina iSelect genotyping array (iCOGs) platform. We also reveal genes that have STRs and which are also differentially regulated by androgens and/or therapeutic anti-androgens. The expansion of STRs within critical prostate cancer genes can potentially affect a man’s risk of developing prostate cancer considering other conditions such as Huntington’s disease where the length of STRs in the HTT gene correlates with severity of disease. Thus, we propose that highly polymorphic STRs that are near prostate cancer risk SNPs and within ChIP peaks, or STRs which are highly expressed in critical PCa genes should be prioritised for future case-control association studies. Finally, we propose that STRs are functional elements of the prostate cancer phenotype, and that these repetitive regions of the genome may account for some of the missing prostate cancer heritability.