In polycystic ovary syndrome models, ovarian TLR4 expression, as well as serum anti-Müllerian hormone, testosterone, caspase1, IL-1β, and insulin levels were increased.330–332 Mechanistically, activation of NLRP3 in upregulated the 3β-hydroxysteroid dehydrogenase and androgen receptor (AR) expression and downregulated the follicle-stimulating hormone receptor expression, inhibition of NLRP3 suppressed the expression of ASC, GSDMD-C, and AR.331 These results indicate that activating the NLRP3 inflammasome is crucial for the progression of hyperandrogen-induced polycystic ovary syndrome. This evidence concerns the gene IL1B and polycystic ovary syndrome.