Toll-like receptors are key players in initiation of innate immune response of the host. In addition to innate immunity they can also induce adaptive immune responses. The concept that inflammation can promote chronic prostatic diseases, such as benign prostatic hyperplasia or prostate carcinoma is supported by several new findings. Epidemiological data have correlated prostatitis with an increased risk of prostate cancer, while PCR-based analyses of bacterial colonization in prostate cancer specimens and normal prostate tissue showed high correlation of bacterial colonization and chronic inflammation with a diagnosis of prostate carcinoma. Even evidence from genetic studies support the hypothesis that prostate inflammation may be a cause of prostate cancer. From these points of view identification of factors, such as SNPs in TLR genes, associated with risk for prostate carcinoma development seems reasonable. Consequently, there are many investigations showing the connection between SNPs in TLR genes and pronounced susceptibility to different diseases. In this article we review the key findings about the genetic variability of TLR genes and prostate cancer risk.