This may explain the fact that in UC the cell’s defence mechanisms protect it against apoptosis to a greater degree by increasing anti-apoptotic BCL2. These results may be supported by research carried out by Sventoraityte et al. [14], which demonstrated that in IBD patients the imbalance between production of pro-inflammatory Th1 and anti-inflammatory Th2 cytokines persists even during remission of the disease, and disturbances of immune homeostasis are significantly more expressed in patients with CD than in patients with UC. Here, BCL2 is linked to inflammatory bowel disease.