Genetic variants that may also lead to an increased risk of Crohn’s disease are linked to Toll-like receptor 4 (TLR-4), typically responsible for recognizing bacterial lipopolysaccharide, CARD9 (caspase recruitment domain-containing protein 9), engaged in defense against pathogens such as yeasts, and interleukin 23 receptor (IL-23R), while IL-23 has been implicated in inhibiting the development of regulatory T cell development in the intestine (Liu and Anderson, 2014; Manuc et al., 2016). This evidence concerns the gene TLR4 and Crohn disease.