The work of Shi et al. showed that dimethyl fumarate promoted NLRP3 phosphorylation on Ser/Thr residues at specific sites of protein kinase A (PKA) and enhanced PKA signaling to inhibit NLRP3 inflammasome activation, pyroptosis, and IL-1 β Secretion, thereby treating Con A-induced AIH [173]. This evidence concerns the gene NLRP3 and autoimmune hepatitis.