In vitro, βOHB inhibits HDAC1 and enhances histone H3 acetylation in macrophages through binding to GPCRs, which results in increased FOXP3+ gene expression and inhibited NOD-like receptor pyrin-domain containing-3 (NLRP3) inflammasome activation, which could, in turn, inhibit the expression of pro-inflammatory cytokines involved in IBD [71]. Here, NLRP3 is linked to inflammatory bowel disease.