Ulcerative colitis is a major type of inflammatory bowel disease characterized by chronic idiopathic mucosal inflammation in the rectum to the colon. Patients with ulcerative colitis exhibit a life expectancy of five years shorter than the general population, and within five years of diagnosis, 7% undergo colectomy. As of 2023, the global prevalence of ulcerative colitis is estimated to be higher than five million cases, and the incidence rate is increasing. However, the precise etiology remains unclear.1 A previous genome-wide association study (GWAS) reported that the ring finger protein 186 gene (RNF186) is a potent pathogenesis-related factor of ulcerative colitis. RNF186 protein plays a pivotal role in intestine homeostasis through the regulation of the expression of occludin, a major gut barrier component, by polyubiquitination. Moreover, the colitis symptoms of RNF186 gene knockout mice were more severe compared with wild-type mice. In addition, the two genetic variants A64T (rs41264113) and R179X (rs36095412) that result in an altered form of RNF186 protein were shown to be associated with the pathomechanism of ulcerative colitis in a Caucasian population.2,3 Additionally, both the A64T and R179X variants result in changes in amino acids in the protein. However, the A64T variant confers susceptibility to ulcerative colitis, while the R179X variant confers resistance to ulcerative colitis.