FOXP3 and autoimmune disease: Although inhibiting EZH2 activity in Tregs can enhance the proinflammatory function of Tregs, alleviate the inhibition of Tregs on the recruitment and function of CD8+ and CD4+ effector T cells, and consequently reshape the TME, there is a potential risk of autoimmune diseases due to disruption in FOXP3-EZH2 interaction (150, 151).