Existing research suggests that multiple factors, including infection, abnormal intrauterine pressure, nutritional factors, psychosocial influences, genetics, and apoptosis, are implicated in the pathogenesis of PROM.[6–8] Notably, recent studies have demonstrated the involvement of fractalkinin, a potent proinflammatory factor, in the development of PROM.[9] Furthermore, investigations have revealed increased activation of inflammasomes, including NLRP1, nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3), AIM2, and NLRC4, in cases of PROM. This evidence concerns the gene NLRP3 and infection.