The possible explanations were as follows: (1) lnc-ITSN1-2 positively regulated IL-23R (validated in our following in vitro experiments) which was a key regulator of immune response and inflammation, thus lnc-ITSN1-2 was upregulated and positively correlated with disease activity and inflammation indexes in IBD patients. This evidence concerns the gene IL23R and inflammatory bowel disease.