Mendelian randomization analyses have used single-nucleotide polymorphisms in CRP and/or genetic scores thereof as instruments of the circulating CRP concentrations in order to correct for potential biases of the observational association and have generally reported null results [50, 53, 54], except for a study in EPIC where genetically twofold higher CRP concentrations were associated with higher risk of CRC, but this result lost nominal statistical significance using alternative definitions of instrumental variables [49]. Here, CRP is linked to colorectal carcinoma.