It seems that Blastocystis infection could affect the following pathways: infection-mediated inflammation, increased oxidative stress, and disruption of epithelial TJs through targeting epithelial ZO-1 and producing cathepsin B. The previous pathways are risk factors for CRC development; however, the direct cause of CRC by Blastocystis infection needs further investigation. This evidence concerns the gene TJP1 and Blastocystis infectious disease.