These observations are supported by the significant associations found between CRC prevalence and the intake of some nutrients and nutraceuticals potentially involved in the molecular mechanisms of cancerogenesis, as well as the presence of several nutrigenomic polymorphisms, namely, those involved in folate metabolism (e.g., methylenetetrahydrofolate reductase produced by MTHFR), lipid metabolism (e.g., apolipoprotein A-I [ApoA-I]), oxidative stress (e.g., catalase), and inflammatory (e.g., tumor necrosis factor alpha [TNF-alpha]) responses [1]. This evidence concerns the gene APOA1 and colorectal carcinoma.