Although it has been found that the loss of F. prausnitzii was closely related to the severity of colitis [42] and it might regulate Th17 and Treg cells’ differentiation by inhibiting histone deacetylase 3 and producing butyrate in experimental colitis models [42,43,44], few studies explore the regulation effect of F. prausnitzii on CD4+ T cell differentiation in patients with UC and its mechanism. The gene discussed is CD4; the disease is colitis.