Correspondingly, Zheng et al. [28] demonstrated that in animal models of colitis, PRMT5 targeting reduces bowel expression of IL1B, TNFA, and IL6. Moreover, they showed PRMT5 inhibition to reduce IFNγ production by effector T-cells as well as to increase the number and improve functionality of Tregs, both in mice and humans, clearly linking PRMT5 with UC pathogenesis. Here, IL6 is linked to colitis.