One of these studies [55], using LC-MS/MS, provided novel insights into the molecular pathogenesis of IBD by reporting the involvement, in IBD, of cell adhesion proteins such as CD38, whose abundance was higher in both CD and UC patients than in controls, and of proteins regulating blood pressure, such as angiotensin-converting enzymes 1 and 2 that showed higher levels in CD than in UC [55]. The gene discussed is CD38; the disease is inflammatory bowel disease.