Interestingly, the blockade of Ser198 phosphorylation by mutating Ser198Ala or inhibiting JNK1 in a CAPS mouse model, prevents the Lipopolysaccharide (LPS)-induced CAPS-associated NLRP3 activation, confirming that phosphorylation at Ser198 residue constitutes an essential priming event for NLRP3 inflammasome activation and suggesting that JNK1 inhibition could be considered a promising potential target for CAPS or other NLRP3-related diseases (44). The gene discussed is MAPK8; the disease is cryopyrin-associated periodic syndrome.