Several studies argue against Caspase‐1 instigating pyroptosis in neutrophils.[126, 127] Instead, neutrophils appear to evade Caspase‐1‐mediated pyroptosis, ensuring sustained cytokine production at infection sites while maintaining their primary antimicrobial capabilities.[126] In both human and mouse neutrophils, the TLR4 agonist LPS upregulates NLRP3 and NLRC4, leading to significant IL‐1β secretion. The gene discussed is IL1B; the disease is infection.