For instance, in active ulcerative colitis patients, there is an upregulation of SPARC mRNA levels and protein expression which significantly correlates with histological activity, making it a potential marker for intestinal inflammation.[15] SPARC knockout leads to significant alleviation of disease progression in a 2,4,6‐trinitrobenzene sulfonic acid (TNBS)‐induced colitis mice‐induced mouse model of enteritis by impacting the differentiation of intestinal Th17 cells.[16] However, whether SPARC is involved in modulating the intestinal barrier and CD has not been determined. The gene discussed is SPARC; the disease is Cowden disease.