Chronic, recurrent inflammation that primarily affects the intestines but can also impact several organ systems is known as inflammatory bowel disease (IBD). (Baumgart and Le Berre, 2021, Greuter and Vavricka, 2019) The occurrence and development of IBD are the result of many factors. (Seyedian et al., 2019) It is currently incurable and has a major effect on patient mortality, and long-term chronic inflammation raises the likelihood of various malignant processes that call for lifetime treatment to halt or slow their progression. (Das, 1999, Kobayashi et al., 2020, Shah and Itzkowitz, 2022) IBD is a serious health issue that affects people all around the world. Its high incidence, lifetime medication requirements, and need for testing add up to enormous costs for the healthcare system. (Alonso-Abreu et al., 2020) Therefore, it is vital to better understand the causes of IBD and to create effective treatments.

To explain genetic changes in phenotypes without altering genotypes, the term "epigenetics" was coined in 1942. (Nebbioso et al., 2018) Epigenetic control of autophagy, the immune system, and the intestinal epithelial barrier plays a significant role in the pathogenesis of IBD. (Ray and Longworth, 2019, Zeng et al., 2019) M6A is a highly dynamic and reversible methylation alteration of the mRNA's 6th n-position adenosine that can be cooperatively controlled by writers, erasers, and readers. (Uddin et al., 2021, Zhang et al., 2016) M6A, a significant epigenetic, may influence post-transcriptional gene regulation to contribute to the onset and progression of IBD. (Lu et al., 2020) On the one hand, m6A can control intestinal epithelial cell apoptosis, intestinal mucosal immunity, and the mucosal barrier. However, m6A can also react when the gut microbiota and their metabolites are out of balance, It is very important in IBD. (Amatullah and Jeffrey, 2020, Zhang et al., 2023) This review covers the precise alterations and functions of m6A in the etiology of IBD and offers fresh perspectives and recommendations for further research into the disease. Here, we summarized m6A roles in the pathogenesis of IBD. (Fig. 1)