Antioxidant/redox pathway genetic variation combined with Se status interactions was associated with a significant effect on CRC risk (P = 0.011 and 0.010 for Se and SELENOP interactions, respectively), possibly driven by SNPs in HIF1A, KEAP1, GPX7, CAT, and SOD2 (when considering the P-values for each individual gene regarding gene only variation and gene x Se status interaction; see Supplementary Table S5). This evidence concerns the gene KEAP1 and colorectal carcinoma.