Furthermore, the metabolites of beneficial gut microbiota such as intestinal SCFA (acetate and butyrate) can modulate histone deacetylase inhibitor (HDACi) function, mediating the decondensation and relaxation of chromatin, in which butyrate plays a protective role against T1D, by enhancing β-cells proliferation, leading to an enhanced gene expression of insulin in human and rat pancreatic β-cells [19,91,199,200,210,211]. The gene discussed is INS; the disease is type 1 diabetes mellitus.