One previous study reported that the loss of NLRP3 inflammasome activity in neutrophils could alleviate gout symptoms.25 Another study found that MSU formation exacerbated NLRP3 inflammasome activation, thereby promoting gout development.26 Further animal experiments demonstrated that IL-17A could aggravate MSU-induced NLRP3 inflammasome formation and that the miR-23a mimic could reverse this effect. This evidence concerns the gene IL17A and gout.