Past studies showed reduced PTPN22 expression in the gastrointestinal tract of patients with Crohn’s disease [22], and PTPN22 deficiency caused: increased secretion of interleukin-6 (IL-6) and IL-8, increased activation of p38 and c-Jun N-terminal kinase (JNK), increased phosphorylation of nuclear factor κB (NF-kB) p65, and increased autophagy, all which could lead to prolonged survival of activated macrophage and promote inflammatory condition in Crohn’s disease [23]. This evidence concerns the gene NFKB1 and Crohn disease.