Published KRX-0401 studies have reported that polymorphisms in IFNGR1 are significantly associated with susceptibility of chronic hepatitis B virus infection, early gastric carcinoma, and rectal cancer. In this study, we found the minor allele of rs2234711 in the promoter of IFNGR1 to be associated with an increased risk of CRC. Rs2234711 has also been reported to be associated with the susceptibility of early gastric carcinoma, chronic hepatitis B virus infection and cerebral malaria. A previous study indicated that rs2234711 may have functional effects on stimulating B cell lines, and C allele was associated with decreased IFNGR1 gene activity, however, in a context-dependent manner. Rs2234711 is located near an activating protein -2/AP-4 consensus binding site and overexpression of AP-2a has been shown to reduce the expression of IFNGR1 and to inhibit IFNG signaling. Moreover, rs2234711 is located in the binding site of POLB, which has been associated with CRC. Together with evidences above, our finding suggested that the functional variant rs2234711 might have an effect on CRC causation through regulating the expression or function of IFNGR1. The only gene showing association in both studies was IFNGR1, however, the SNP rs2234711 which was associated with CRC risk in our study, was not covered by any tagSNP in the previous study. For the risk analysis, both studies were large. There may be small differences in the origin of the study participants, with our study coming from a genetically quite uniform Czech population, while the recruitment area of the study by Slattery et. al. was Northern California and Utah, including also some 10–20% of Hispanic, Black and Asian participants. For the survival analysis, the studies had comparable follow-up time, but while Slattery et. al. had follow-up for all patients, we had it only for 483 patients, which decreased our power to detect small associations. However, this ensured that only newly diagnosed CRC cases were included in our study, excluding a survival bias. For this subgroup, nearly complete clinical data were available, allowing evaluation of the SNPs as independent prognostic markers. GWASs mainly describe only the most robust associations, which may be the reason that they have not reported any associations between CRC and interferon pathway genes. The tagSNP approach, used in the GWAS, is thought as a method with maximum SNP prediction accuracy, however, it does not cover all SNPs in the regulatory regions. A total of 74 SNPs in the regulatory and coding regions of the genes were covered by our study. It is possible that SNPs with a lower MAF or SNPs in still unknown regulatory regions of the studied genes, such as the enhancer and the silencer regions, might also modulate CRC susceptibility or survival. In summary, our results, together with the previous study.