Overall, our analyses suggest that genetic variation in TGF beta signaling (pathway 7), which includes members such as BMP2, BMPR2, SMAD3, and SMAD7 implicated in CRC risk by previous large case-control and GWAS reports [36,37,38], is sufficient to alter CRC risk, independent of Se status interaction, while SNP risk associations attributed to the antioxidant and apoptosis pathways may be significantly modified by Se status interactions. The gene discussed is SMAD3; the disease is colorectal carcinoma.