When evaluating the best evidence for optimizing treatment of inflammatory bowel disease (IBD), the focus is usually on anti-inflammatory drugs and treatments that modulate the immune system. The intestinal immune response remains key to the development of therapeutic approaches. Over the past decade, the concept of gut microbial imbalance has emerged as a potential pathogenic focus for IBD, and there has been a gradual increase in scholarly interest in controlling gut microbes as the primary approach to controlling the disease. Meihua Xu, Department of Gastroenterology, Xiangya Hospital, Central South University In this review, anti-inflammatory, immunomodulatory, and microbial regulatory therapies are included as part of the treatment that may become a therapeutic medical device in the near future. As our understanding of the underlying biology of IBD evolves, the disconnect between a patient’s symptoms and inflammatory disease continues to receive attention. As clinical trials address both symptom scoring and mucosal healing, researchers and clinicians are beginning to understand that many symptoms may not be caused by active inflammation and therefore focusing solely on immunomodulatory therapy will not fully meet the needs of the patient. In addition, there is a growing recognition of the importance of stress and mental health to symptom improvement and treatment needs. In this review, the improvement of patient symptoms and other approaches used to enhance patient well-being will also be discussed. Finally, throughout the article, important research questions regarding different aspects of treatment will be presented. The combined oral and transrectal application of 5-ASA is more effective than alone in the treatment of active ulcerative colitis. In addition, although there is limited data demonstrating that the maximum dose is more effective than at least 2 g per day, do not be afraid to take the maximum oral dose of 5-ASA as it is very safe. When mild to moderately active ulcerative colitis or Crohn’s lesions are corticosteroid-dependent, thiopurines (azathioprine and 6-mercaptopurine) may be used to maintain disease remission. Before starting thiopurine therapy, thiopurine methyl levels should be tested to ensure that they are safe when applied at normal doses. For patients with corticosteroid-dependent or corticosteroid-resistant severe ulcerative colitis or Crohn’s disease, or for patients with active Crohn’s disease presenting with fistulae, application of TNF antibodies is an option. Anti-TNF therapy can be optimized with the combination of thiopurine therapy. When a patient with ulcerative colitis or Crohn’s disease becomes symptomatic, it is important to determine whether the symptoms reflect active inflammatory disease. When patients become symptomatic, primary care physicians should avoid prescribing short-acting corticosteroids unless objective indicators demonstrate that their symptoms are caused by disease activity. In addition to clear imaging findings, these indicators can include a decrease in serum hemoglobin and/or albumin, elevated serum C-reactive protein or elevated fecal calcium defense protein. The initial physician will need to take time to explore the patient’s stress and depression, even in the absence of inflammatory disease, where stress, mood and anxiety disorders can cause the patient to become symptomatic. Finally, it is important to identify the cause of severe or persistent pain and to avoid the long-term use of narcotics for pain management because their use is associated with a poor prognosis.